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ezetimibe solutions (MedChemExpress)

Name: ezetimibe solutions
Brand: MedChemExpress
Rating: 93 (15 reviews)

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MedChemExpress ezetimibe solutions

Effects of <t>Ezetimibe</t> on the viability, proliferation, and cell cycle of TNBC cells. (A) Viability of MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 1, 5, 10, 15, 20, 40, 60, 80, 100 μmol/L) for 48 h was detected using the CCK-8 assay. (B) Cell cloning experiments were performed to measure the colony formation of MDA-MB-231 cells after 10 days and 4T1 cells after 14 days of treatment with different concentrations of Ezetimibe (0, 20, 40 μmol/L). (C) Flow cytometry analysis was conducted to examine cell cycle distribution of MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. (D) Western blotting was performed to determine the expression levels of Ki67, CDK2, CDK4, and CyclinD1 proteins in MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Representative results from three independent experiments are shown, and the data are presented as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Ezetimibe Solutions, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Ezetimibe inhibits triple-negative breast cancer proliferation and promotes cell cycle arrest by targeting the PDGFR/AKT pathway"

Article Title: Ezetimibe inhibits triple-negative breast cancer proliferation and promotes cell cycle arrest by targeting the PDGFR/AKT pathway

Journal: Heliyon

doi: 10.1016/j.heliyon.2023.e21343

Effects of Ezetimibe on the viability, proliferation, and cell cycle of TNBC cells. (A) Viability of MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 1, 5, 10, 15, 20, 40, 60, 80, 100 μmol/L) for 48 h was detected using the CCK-8 assay. (B) Cell cloning experiments were performed to measure the colony formation of MDA-MB-231 cells after 10 days and 4T1 cells after 14 days of treatment with different concentrations of Ezetimibe (0, 20, 40 μmol/L). (C) Flow cytometry analysis was conducted to examine cell cycle distribution of MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. (D) Western blotting was performed to determine the expression levels of Ki67, CDK2, CDK4, and CyclinD1 proteins in MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Representative results from three independent experiments are shown, and the data are presented as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Figure Legend Snippet: Effects of Ezetimibe on the viability, proliferation, and cell cycle of TNBC cells. (A) Viability of MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 1, 5, 10, 15, 20, 40, 60, 80, 100 μmol/L) for 48 h was detected using the CCK-8 assay. (B) Cell cloning experiments were performed to measure the colony formation of MDA-MB-231 cells after 10 days and 4T1 cells after 14 days of treatment with different concentrations of Ezetimibe (0, 20, 40 μmol/L). (C) Flow cytometry analysis was conducted to examine cell cycle distribution of MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. (D) Western blotting was performed to determine the expression levels of Ki67, CDK2, CDK4, and CyclinD1 proteins in MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Representative results from three independent experiments are shown, and the data are presented as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Techniques Used: CCK-8 Assay, Clone Assay, Flow Cytometry, Western Blot, Expressing, Standard Deviation

Effects of Ezetimibe on the transcriptome of TNBC cells and its impact on levels of PDGFRβ mRNA and protein. (A) MDA-MB-231 cells were treated with 20 μM Ezetimibe for 48 h, followed by transcriptome sequencing. Genes with fold change >2 for upregulation and <0.6 for downregulation were selected as differentially expressed genes between the 20 μM Ezetimibe treatment group and the control group. (B) Volcano plot of differential genes in(A). (C) and (D) Gene Ontology was utilized to extract and merge enriched pathways, and the distribution of enriched q-values for each pathway was plotted. (C) Represents the pathway enrichment analysis for the upregulated genes in (A), while (D) represents the pathway enrichment analysis for the downregulated genes in (A). (E) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the mRNA levels of PDGFRβ were measured using qRT-PCR. (F) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the expression of PDGFRβ protein was assessed using Western blot. The representative results shown in the figure are the mean ± standard deviation (Mean ± SD) of three independent experiments: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Figure Legend Snippet: Effects of Ezetimibe on the transcriptome of TNBC cells and its impact on levels of PDGFRβ mRNA and protein. (A) MDA-MB-231 cells were treated with 20 μM Ezetimibe for 48 h, followed by transcriptome sequencing. Genes with fold change >2 for upregulation and <0.6 for downregulation were selected as differentially expressed genes between the 20 μM Ezetimibe treatment group and the control group. (B) Volcano plot of differential genes in(A). (C) and (D) Gene Ontology was utilized to extract and merge enriched pathways, and the distribution of enriched q-values for each pathway was plotted. (C) Represents the pathway enrichment analysis for the upregulated genes in (A), while (D) represents the pathway enrichment analysis for the downregulated genes in (A). (E) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the mRNA levels of PDGFRβ were measured using qRT-PCR. (F) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the expression of PDGFRβ protein was assessed using Western blot. The representative results shown in the figure are the mean ± standard deviation (Mean ± SD) of three independent experiments: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Techniques Used: Sequencing, Control, Quantitative RT-PCR, Expressing, Western Blot, Standard Deviation

The impact of PDGFRβ overexpression on the inhibition of MDA-MB-231 and 4T1 cell proliferation and the ability of Ezetimibe to arrest the cell cycle. (A) (B) qRT-PCR and Western blotting were respectively performed to detect the mRNA and protein levels of PDGFRβ in PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, respectively, as well as in the control group cells. (C) PDGFRβ-overexpressing or vector-transfected MDA-MB-231 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 10 days, while PDGFRβ-overexpressing or vector-transfected 4T1 cells were treated for 14 days. The cell clone formation experiment was conducted to determine the number of cell clones formed. (D) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as vector-transfected control cells, were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h, and flow cytometry was used to detect the cell cycle distribution. (E) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as vector-transfected control group cells, were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Western blotting was used to examine the expression of Ki67, CDK2, CDK4, and Cyclin D1 proteins. (F) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as vector-transfected control group cells, were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Western blotting was performed to analyze the expression of PDGFRβ, t -AKT, and p -AKT473 proteins. The results presented in the figure are representative of three independent experiments and are expressed as the mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01,***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Figure Legend Snippet: The impact of PDGFRβ overexpression on the inhibition of MDA-MB-231 and 4T1 cell proliferation and the ability of Ezetimibe to arrest the cell cycle. (A) (B) qRT-PCR and Western blotting were respectively performed to detect the mRNA and protein levels of PDGFRβ in PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, respectively, as well as in the control group cells. (C) PDGFRβ-overexpressing or vector-transfected MDA-MB-231 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 10 days, while PDGFRβ-overexpressing or vector-transfected 4T1 cells were treated for 14 days. The cell clone formation experiment was conducted to determine the number of cell clones formed. (D) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as vector-transfected control cells, were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h, and flow cytometry was used to detect the cell cycle distribution. (E) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as vector-transfected control group cells, were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Western blotting was used to examine the expression of Ki67, CDK2, CDK4, and Cyclin D1 proteins. (F) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as vector-transfected control group cells, were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Western blotting was performed to analyze the expression of PDGFRβ, t -AKT, and p -AKT473 proteins. The results presented in the figure are representative of three independent experiments and are expressed as the mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01,***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Techniques Used: Over Expression, Inhibition, Quantitative RT-PCR, Western Blot, Control, Plasmid Preparation, Transfection, Clone Assay, Flow Cytometry, Expressing, Standard Deviation

The effects of AKT activation on the inhibition of MDA-MB-231 and 4T1 cell proliferation and cell cycle arrest by Ezetimibe. (A) MDA-MB-231 and 4T1 cells were treated with different concentrations of SC79 (0, 0.5, 1, 5, 10, 15, 20, 40 μmol/L) for 48 h, and cell viability was measured using the CCK-8 assay. (B) MDA-MB-231 and 4T1 cells were treated with SC79 (0, 10 μmol/L) for 48 h, and the levels of t -AKT and p -AKT473 were detected using Western blotting analysis. (C) MDA-MB-231 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 10 days, and 4T1 cells were treated for 14 days. The cell colony formation assay was used to measure the number of cell colonies formed. (D) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 48 h, and cell cycle distribution was analyzed using flow cytometry. (E) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 48 h, and the expression levels of Ki67, CDK2, CDK4, and CyclinD1 proteins were determined by Western blotting analysis. (F) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 48 h, and the levels of PDGFRβ, t -AKT, and p -AKT473 proteins were measured by Western blotting analysis. The results shown in the figure are representative of three independent experiments and are presented as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe, SC79 or other chemicals refers to 0.1 % (v/v) DMSO solution.

Figure Legend Snippet: The effects of AKT activation on the inhibition of MDA-MB-231 and 4T1 cell proliferation and cell cycle arrest by Ezetimibe. (A) MDA-MB-231 and 4T1 cells were treated with different concentrations of SC79 (0, 0.5, 1, 5, 10, 15, 20, 40 μmol/L) for 48 h, and cell viability was measured using the CCK-8 assay. (B) MDA-MB-231 and 4T1 cells were treated with SC79 (0, 10 μmol/L) for 48 h, and the levels of t -AKT and p -AKT473 were detected using Western blotting analysis. (C) MDA-MB-231 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 10 days, and 4T1 cells were treated for 14 days. The cell colony formation assay was used to measure the number of cell colonies formed. (D) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 48 h, and cell cycle distribution was analyzed using flow cytometry. (E) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 48 h, and the expression levels of Ki67, CDK2, CDK4, and CyclinD1 proteins were determined by Western blotting analysis. (F) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 48 h, and the levels of PDGFRβ, t -AKT, and p -AKT473 proteins were measured by Western blotting analysis. The results shown in the figure are representative of three independent experiments and are presented as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe, SC79 or other chemicals refers to 0.1 % (v/v) DMSO solution.

Techniques Used: Activation Assay, Inhibition, CCK-8 Assay, Western Blot, Colony Assay, Flow Cytometry, Expressing, Standard Deviation

The impact of MK2206 on the inhibitory effect on the proliferation and cell cycle arrest of PDGFRβ overexpressing TNBC cells by Ezetimibe. (A) MDA-MB-231 and 4T1 cells overexpressing PDGFRβ or transfected with empty vector were treated with different concentrations of MK2206 (0, 0.5, 1, 5, 10, 15, 20, 40 μmol/L) for 48 h, and cell viability was measured using the CCK-8 assay. (B) MDA-MB-231 and 4T1 cells were treated with MK2206 (0, 1 μmol/L) for 48 h, and the expression of t -AKT and p -AKT473 was examined by Western blot. (C) MDA-MB-231 cells overexpressing PDGFRβ or transfected with empty vector were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 10 days, and 4T1 cells were treated for 14 days. Cell clony formation was assessed by colony formation assay. (D) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as control cells, were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 48 h, and cell cycle distribution was analyzed by flow cytometry. (E) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as control cells, were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the expression of Ki67, CDK2, CDK4, and CyclinD1 proteins was examined by Western blot. (F) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as control cells, were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the expression of PDGFRβ, t -AKT, and p -AKT473 proteins was examined by Western blot. The results shown in the figures represent the mean ± standard deviation (Mean ± SD) of three independent experiments. Statistical significance is denoted as: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe, MK2206 or other chemicals refers to 0.1 % (v/v) DMSO solution.

Figure Legend Snippet: The impact of MK2206 on the inhibitory effect on the proliferation and cell cycle arrest of PDGFRβ overexpressing TNBC cells by Ezetimibe. (A) MDA-MB-231 and 4T1 cells overexpressing PDGFRβ or transfected with empty vector were treated with different concentrations of MK2206 (0, 0.5, 1, 5, 10, 15, 20, 40 μmol/L) for 48 h, and cell viability was measured using the CCK-8 assay. (B) MDA-MB-231 and 4T1 cells were treated with MK2206 (0, 1 μmol/L) for 48 h, and the expression of t -AKT and p -AKT473 was examined by Western blot. (C) MDA-MB-231 cells overexpressing PDGFRβ or transfected with empty vector were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 10 days, and 4T1 cells were treated for 14 days. Cell clony formation was assessed by colony formation assay. (D) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as control cells, were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 48 h, and cell cycle distribution was analyzed by flow cytometry. (E) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as control cells, were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the expression of Ki67, CDK2, CDK4, and CyclinD1 proteins was examined by Western blot. (F) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as control cells, were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the expression of PDGFRβ, t -AKT, and p -AKT473 proteins was examined by Western blot. The results shown in the figures represent the mean ± standard deviation (Mean ± SD) of three independent experiments. Statistical significance is denoted as: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe, MK2206 or other chemicals refers to 0.1 % (v/v) DMSO solution.

Techniques Used: Transfection, Plasmid Preparation, CCK-8 Assay, Expressing, Western Blot, Colony Assay, Control, Flow Cytometry, Standard Deviation

The effects of Ezetimibe on TNBC growth and the PDGFRβ/AKT pathway in vivo. (A) MDA-MB-231 cells overexpressing PDGFRβ or transfected with empty vector were separately used to establish subcutaneous breast tumor models in mice. When the tumors reached a size of 5 mm in length, the mice were randomly divided into 8 groups, with 5 mice in each group. The groups received the following treatments: LVCONTROL (empty vector MDA-MB-231) with vehicle treatment, LVCONTROL + ezetimibe (empty vector MDA-MB-231) treated with ezetimibe alone, LVPDGFRB (PDGFRβ-overexpressing MDA-MB-231) with vehicle treatment, LVPDGFRB + ezetimibe (PDGFRβ-overexpressing MDA-MB-231) treated with ezetimibe alone, LVPDGFRB + MK2206 (PDGFRβ-overexpressing MDA-MB-231) treated with MK2206 alone, LVPDGFRB + ezetimibe + MK2206 (PDGFRβ-overexpressing MDA-MB-231) treated with the combination of ezetimibe and MK2206, LVCONTROL + SC79 (empty vector MDA-MB-231) treated with SC79 alone, and LVCONTROL + ezetimibe + SC79 (empty vector MDA-MB-231) treated with the combination of ezetimibe and SC79. During the treatment process, the body weight (A) and tumor length and width (B) were measured at regular intervals. The tumor volume was calculated using the formula: length × width 2 /2. (C) When the tumor volume reached 2000 mm 3 , the mice were euthanized while under anesthesia, and the tumors were harvested and photographed. (D) Tumors from xenograft mice with breast cancer were harvested when they reached a size of 2000 mm 3 . Immunohistochemical staining was performed on the xenograft tumors from each group to detect the expression levels of Ki67, CDK2, CDK4, and CyclinD1. Representative images were captured under a microscope at a magnification of × 400. (E) Immunohistochemical staining was performed on the xenograft tumors from each group to detect the expression levels of PDGFRβ, AKT, and p -AKT473. Representative images were captured under a microscope at a magnification of × 400. The results presented in the figures are representative of three independent experiments and are expressed as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Figure Legend Snippet: The effects of Ezetimibe on TNBC growth and the PDGFRβ/AKT pathway in vivo. (A) MDA-MB-231 cells overexpressing PDGFRβ or transfected with empty vector were separately used to establish subcutaneous breast tumor models in mice. When the tumors reached a size of 5 mm in length, the mice were randomly divided into 8 groups, with 5 mice in each group. The groups received the following treatments: LVCONTROL (empty vector MDA-MB-231) with vehicle treatment, LVCONTROL + ezetimibe (empty vector MDA-MB-231) treated with ezetimibe alone, LVPDGFRB (PDGFRβ-overexpressing MDA-MB-231) with vehicle treatment, LVPDGFRB + ezetimibe (PDGFRβ-overexpressing MDA-MB-231) treated with ezetimibe alone, LVPDGFRB + MK2206 (PDGFRβ-overexpressing MDA-MB-231) treated with MK2206 alone, LVPDGFRB + ezetimibe + MK2206 (PDGFRβ-overexpressing MDA-MB-231) treated with the combination of ezetimibe and MK2206, LVCONTROL + SC79 (empty vector MDA-MB-231) treated with SC79 alone, and LVCONTROL + ezetimibe + SC79 (empty vector MDA-MB-231) treated with the combination of ezetimibe and SC79. During the treatment process, the body weight (A) and tumor length and width (B) were measured at regular intervals. The tumor volume was calculated using the formula: length × width 2 /2. (C) When the tumor volume reached 2000 mm 3 , the mice were euthanized while under anesthesia, and the tumors were harvested and photographed. (D) Tumors from xenograft mice with breast cancer were harvested when they reached a size of 2000 mm 3 . Immunohistochemical staining was performed on the xenograft tumors from each group to detect the expression levels of Ki67, CDK2, CDK4, and CyclinD1. Representative images were captured under a microscope at a magnification of × 400. (E) Immunohistochemical staining was performed on the xenograft tumors from each group to detect the expression levels of PDGFRβ, AKT, and p -AKT473. Representative images were captured under a microscope at a magnification of × 400. The results presented in the figures are representative of three independent experiments and are expressed as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Techniques Used: In Vivo, Transfection, Plasmid Preparation, Immunohistochemical staining, Staining, Expressing, Microscopy, Standard Deviation

Image Search Results

Journal: Heliyon

Article Title: Ezetimibe inhibits triple-negative breast cancer proliferation and promotes cell cycle arrest by targeting the PDGFR/AKT pathway

doi: 10.1016/j.heliyon.2023.e21343

Figure Lengend Snippet: Effects of Ezetimibe on the viability, proliferation, and cell cycle of TNBC cells. (A) Viability of MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 1, 5, 10, 15, 20, 40, 60, 80, 100 μmol/L) for 48 h was detected using the CCK-8 assay. (B) Cell cloning experiments were performed to measure the colony formation of MDA-MB-231 cells after 10 days and 4T1 cells after 14 days of treatment with different concentrations of Ezetimibe (0, 20, 40 μmol/L). (C) Flow cytometry analysis was conducted to examine cell cycle distribution of MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. (D) Western blotting was performed to determine the expression levels of Ki67, CDK2, CDK4, and CyclinD1 proteins in MDA-MB-231 and 4T1 cells treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Representative results from three independent experiments are shown, and the data are presented as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Article Snippet: Ezetimibe solutions for storage and use are prepared by dissolving ezetimibe (MedChemExpress, Catalog #HY-17376) in DMSO.

Techniques: CCK-8 Assay, Clone Assay, Flow Cytometry, Western Blot, Expressing, Standard Deviation

Journal: Heliyon

Article Title: Ezetimibe inhibits triple-negative breast cancer proliferation and promotes cell cycle arrest by targeting the PDGFR/AKT pathway

doi: 10.1016/j.heliyon.2023.e21343

Figure Lengend Snippet: Effects of Ezetimibe on the transcriptome of TNBC cells and its impact on levels of PDGFRβ mRNA and protein. (A) MDA-MB-231 cells were treated with 20 μM Ezetimibe for 48 h, followed by transcriptome sequencing. Genes with fold change >2 for upregulation and <0.6 for downregulation were selected as differentially expressed genes between the 20 μM Ezetimibe treatment group and the control group. (B) Volcano plot of differential genes in(A). (C) and (D) Gene Ontology was utilized to extract and merge enriched pathways, and the distribution of enriched q-values for each pathway was plotted. (C) Represents the pathway enrichment analysis for the upregulated genes in (A), while (D) represents the pathway enrichment analysis for the downregulated genes in (A). (E) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the mRNA levels of PDGFRβ were measured using qRT-PCR. (F) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the expression of PDGFRβ protein was assessed using Western blot. The representative results shown in the figure are the mean ± standard deviation (Mean ± SD) of three independent experiments: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Article Snippet: Ezetimibe solutions for storage and use are prepared by dissolving ezetimibe (MedChemExpress, Catalog #HY-17376) in DMSO.

Techniques: Sequencing, Control, Quantitative RT-PCR, Expressing, Western Blot, Standard Deviation

Journal: Heliyon

Article Title: Ezetimibe inhibits triple-negative breast cancer proliferation and promotes cell cycle arrest by targeting the PDGFR/AKT pathway

doi: 10.1016/j.heliyon.2023.e21343

Figure Lengend Snippet: The impact of PDGFRβ overexpression on the inhibition of MDA-MB-231 and 4T1 cell proliferation and the ability of Ezetimibe to arrest the cell cycle. (A) (B) qRT-PCR and Western blotting were respectively performed to detect the mRNA and protein levels of PDGFRβ in PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, respectively, as well as in the control group cells. (C) PDGFRβ-overexpressing or vector-transfected MDA-MB-231 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 10 days, while PDGFRβ-overexpressing or vector-transfected 4T1 cells were treated for 14 days. The cell clone formation experiment was conducted to determine the number of cell clones formed. (D) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as vector-transfected control cells, were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h, and flow cytometry was used to detect the cell cycle distribution. (E) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as vector-transfected control group cells, were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Western blotting was used to examine the expression of Ki67, CDK2, CDK4, and Cyclin D1 proteins. (F) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as vector-transfected control group cells, were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) for 48 h. Western blotting was performed to analyze the expression of PDGFRβ, t -AKT, and p -AKT473 proteins. The results presented in the figure are representative of three independent experiments and are expressed as the mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01,***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe refers to 0.1 % (v/v) DMSO solution.

Article Snippet: Ezetimibe solutions for storage and use are prepared by dissolving ezetimibe (MedChemExpress, Catalog #HY-17376) in DMSO.

Techniques: Over Expression, Inhibition, Quantitative RT-PCR, Western Blot, Control, Plasmid Preparation, Transfection, Clone Assay, Flow Cytometry, Expressing, Standard Deviation

Journal: Heliyon

Article Title: Ezetimibe inhibits triple-negative breast cancer proliferation and promotes cell cycle arrest by targeting the PDGFR/AKT pathway

doi: 10.1016/j.heliyon.2023.e21343

Figure Lengend Snippet: The effects of AKT activation on the inhibition of MDA-MB-231 and 4T1 cell proliferation and cell cycle arrest by Ezetimibe. (A) MDA-MB-231 and 4T1 cells were treated with different concentrations of SC79 (0, 0.5, 1, 5, 10, 15, 20, 40 μmol/L) for 48 h, and cell viability was measured using the CCK-8 assay. (B) MDA-MB-231 and 4T1 cells were treated with SC79 (0, 10 μmol/L) for 48 h, and the levels of t -AKT and p -AKT473 were detected using Western blotting analysis. (C) MDA-MB-231 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 10 days, and 4T1 cells were treated for 14 days. The cell colony formation assay was used to measure the number of cell colonies formed. (D) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 48 h, and cell cycle distribution was analyzed using flow cytometry. (E) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 48 h, and the expression levels of Ki67, CDK2, CDK4, and CyclinD1 proteins were determined by Western blotting analysis. (F) MDA-MB-231 and 4T1 cells were treated with different concentrations of Ezetimibe (0, 20, 40 μmol/L) and SC79 (0, 10 μmol/L) for 48 h, and the levels of PDGFRβ, t -AKT, and p -AKT473 proteins were measured by Western blotting analysis. The results shown in the figure are representative of three independent experiments and are presented as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe, SC79 or other chemicals refers to 0.1 % (v/v) DMSO solution.

Article Snippet: Ezetimibe solutions for storage and use are prepared by dissolving ezetimibe (MedChemExpress, Catalog #HY-17376) in DMSO.

Techniques: Activation Assay, Inhibition, CCK-8 Assay, Western Blot, Colony Assay, Flow Cytometry, Expressing, Standard Deviation

Journal: Heliyon

Article Title: Ezetimibe inhibits triple-negative breast cancer proliferation and promotes cell cycle arrest by targeting the PDGFR/AKT pathway

doi: 10.1016/j.heliyon.2023.e21343

Figure Lengend Snippet: The impact of MK2206 on the inhibitory effect on the proliferation and cell cycle arrest of PDGFRβ overexpressing TNBC cells by Ezetimibe. (A) MDA-MB-231 and 4T1 cells overexpressing PDGFRβ or transfected with empty vector were treated with different concentrations of MK2206 (0, 0.5, 1, 5, 10, 15, 20, 40 μmol/L) for 48 h, and cell viability was measured using the CCK-8 assay. (B) MDA-MB-231 and 4T1 cells were treated with MK2206 (0, 1 μmol/L) for 48 h, and the expression of t -AKT and p -AKT473 was examined by Western blot. (C) MDA-MB-231 cells overexpressing PDGFRβ or transfected with empty vector were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 10 days, and 4T1 cells were treated for 14 days. Cell clony formation was assessed by colony formation assay. (D) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as control cells, were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 48 h, and cell cycle distribution was analyzed by flow cytometry. (E) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as control cells, were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the expression of Ki67, CDK2, CDK4, and CyclinD1 proteins was examined by Western blot. (F) PDGFRβ-overexpressing MDA-MB-231 and 4T1 cells, as well as control cells, were treated with different concentrations of MK2206 (0, 1 μmol/L) and Ezetimibe (0, 20, 40 μmol/L) for 48 h, and the expression of PDGFRβ, t -AKT, and p -AKT473 proteins was examined by Western blot. The results shown in the figures represent the mean ± standard deviation (Mean ± SD) of three independent experiments. Statistical significance is denoted as: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Here 0 μmol/L Ezetimibe, MK2206 or other chemicals refers to 0.1 % (v/v) DMSO solution.

Article Snippet: Ezetimibe solutions for storage and use are prepared by dissolving ezetimibe (MedChemExpress, Catalog #HY-17376) in DMSO.

Techniques: Transfection, Plasmid Preparation, CCK-8 Assay, Expressing, Western Blot, Colony Assay, Control, Flow Cytometry, Standard Deviation

Journal: Heliyon

Article Title: Ezetimibe inhibits triple-negative breast cancer proliferation and promotes cell cycle arrest by targeting the PDGFR/AKT pathway

doi: 10.1016/j.heliyon.2023.e21343

Figure Lengend Snippet: The effects of Ezetimibe on TNBC growth and the PDGFRβ/AKT pathway in vivo. (A) MDA-MB-231 cells overexpressing PDGFRβ or transfected with empty vector were separately used to establish subcutaneous breast tumor models in mice. When the tumors reached a size of 5 mm in length, the mice were randomly divided into 8 groups, with 5 mice in each group. The groups received the following treatments: LVCONTROL (empty vector MDA-MB-231) with vehicle treatment, LVCONTROL + ezetimibe (empty vector MDA-MB-231) treated with ezetimibe alone, LVPDGFRB (PDGFRβ-overexpressing MDA-MB-231) with vehicle treatment, LVPDGFRB + ezetimibe (PDGFRβ-overexpressing MDA-MB-231) treated with ezetimibe alone, LVPDGFRB + MK2206 (PDGFRβ-overexpressing MDA-MB-231) treated with MK2206 alone, LVPDGFRB + ezetimibe + MK2206 (PDGFRβ-overexpressing MDA-MB-231) treated with the combination of ezetimibe and MK2206, LVCONTROL + SC79 (empty vector MDA-MB-231) treated with SC79 alone, and LVCONTROL + ezetimibe + SC79 (empty vector MDA-MB-231) treated with the combination of ezetimibe and SC79. During the treatment process, the body weight (A) and tumor length and width (B) were measured at regular intervals. The tumor volume was calculated using the formula: length × width 2 /2. (C) When the tumor volume reached 2000 mm 3 , the mice were euthanized while under anesthesia, and the tumors were harvested and photographed. (D) Tumors from xenograft mice with breast cancer were harvested when they reached a size of 2000 mm 3 . Immunohistochemical staining was performed on the xenograft tumors from each group to detect the expression levels of Ki67, CDK2, CDK4, and CyclinD1. Representative images were captured under a microscope at a magnification of × 400. (E) Immunohistochemical staining was performed on the xenograft tumors from each group to detect the expression levels of PDGFRβ, AKT, and p -AKT473. Representative images were captured under a microscope at a magnification of × 400. The results presented in the figures are representative of three independent experiments and are expressed as mean ± standard deviation (Mean ± SD): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: Ezetimibe solutions for storage and use are prepared by dissolving ezetimibe (MedChemExpress, Catalog #HY-17376) in DMSO.

Techniques: In Vivo, Transfection, Plasmid Preparation, Immunohistochemical staining, Staining, Expressing, Microscopy, Standard Deviation

Effects of ezetimibe on metabolic parameters. (A) Body weight. (B) Liver weight shown as a percentage of body weight. (C) Blood glucose level. (D) Plasma insulin level. (E, F) Effect of ezetimibe on oral glucose tolerance. Plasma levels of (G) total triglyceride (TG), (H) total cholesterol (TC), (I) free fatty acids (FFA), and (J) LDL/VLDL. Activities of (K) ALT and (L) AST. Data are expressed as the mean ± SEM ( n = 8 for each group). * p < 0.05, ** p < 0.01 vs. control, by Student’s t-test. Abbreviations: ALT: alanine aminotransferase; AST: aspartate aminotransferase; CONT: control; EZ: ezetimibe; LDL: low-density lipoprotein cholesterol; VLDL: very low-density lipoprotein cholesterol. SEM: standard error of mean.

Journal: Frontiers in Pharmacology

Article Title: Ezetimibe, Niemann-Pick C1 like 1 inhibitor, modulates hepatic phospholipid metabolism to alleviate fat accumulation

doi: 10.3389/fphar.2024.1406493

Figure Lengend Snippet: Effects of ezetimibe on metabolic parameters. (A) Body weight. (B) Liver weight shown as a percentage of body weight. (C) Blood glucose level. (D) Plasma insulin level. (E, F) Effect of ezetimibe on oral glucose tolerance. Plasma levels of (G) total triglyceride (TG), (H) total cholesterol (TC), (I) free fatty acids (FFA), and (J) LDL/VLDL. Activities of (K) ALT and (L) AST. Data are expressed as the mean ± SEM ( n = 8 for each group). * p < 0.05, ** p < 0.01 vs. control, by Student’s t-test. Abbreviations: ALT: alanine aminotransferase; AST: aspartate aminotransferase; CONT: control; EZ: ezetimibe; LDL: low-density lipoprotein cholesterol; VLDL: very low-density lipoprotein cholesterol. SEM: standard error of mean.

Article Snippet: The ezetimibe stock solution was prepared in dimethylsulfoxide (DMSO; Sigma-Aldrich).

Techniques: Control

Effects of ezetimibe on hepatic fat accumulation. Hepatic levels of (A) total triglyceride (TG), (B) total cholesterol (TC), and (C) free fatty acids (FFA) ( n = 8 for each group). (D) Representative H&E-stained liver sections (scale bar, 100 µm). Digital images were captured with an Olympus BX51 light microscope (Tokyo, Japan). (E) Evaluation of NAFLD activity score (NAS). A pathologist blinded to the experimental conditions evaluated the NAFLD activity score (NAS). NAS was calculated as the sum of scores for steatosis (0–3), ballooning (0–2), and inflammation (0–3) ( n = 8 for each group). (F, G) Quantitative analysis of the average of the lipid droplet number (F) and distribution of lipid droplets in diameter (G) ( n = 6 for each group). Each data point is an average of 3 different fields of view per rat. The diameter of lipid droplets (LDs) was measured using ImageJ software. Data are expressed as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. control, by Student’s t-test. Abbreviations: EZ: ezetimibe; H&E: hematoxylin and eosin; NAFLD: non-alcoholic fatty liver disease; NAS: NAFLD activity score; SEM: standard error of mean; TG: triglyceride.

Journal: Frontiers in Pharmacology

Article Title: Ezetimibe, Niemann-Pick C1 like 1 inhibitor, modulates hepatic phospholipid metabolism to alleviate fat accumulation

doi: 10.3389/fphar.2024.1406493

Figure Lengend Snippet: Effects of ezetimibe on hepatic fat accumulation. Hepatic levels of (A) total triglyceride (TG), (B) total cholesterol (TC), and (C) free fatty acids (FFA) ( n = 8 for each group). (D) Representative H&E-stained liver sections (scale bar, 100 µm). Digital images were captured with an Olympus BX51 light microscope (Tokyo, Japan). (E) Evaluation of NAFLD activity score (NAS). A pathologist blinded to the experimental conditions evaluated the NAFLD activity score (NAS). NAS was calculated as the sum of scores for steatosis (0–3), ballooning (0–2), and inflammation (0–3) ( n = 8 for each group). (F, G) Quantitative analysis of the average of the lipid droplet number (F) and distribution of lipid droplets in diameter (G) ( n = 6 for each group). Each data point is an average of 3 different fields of view per rat. The diameter of lipid droplets (LDs) was measured using ImageJ software. Data are expressed as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. control, by Student’s t-test. Abbreviations: EZ: ezetimibe; H&E: hematoxylin and eosin; NAFLD: non-alcoholic fatty liver disease; NAS: NAFLD activity score; SEM: standard error of mean; TG: triglyceride.

Article Snippet: The ezetimibe stock solution was prepared in dimethylsulfoxide (DMSO; Sigma-Aldrich).

Techniques: Staining, Light Microscopy, Activity Assay, Software, Control

Metabolomic and lipidomic analyses. (A, B) Principal component analysis (PCA) (A) and orthogonal partial least squares discriminant analysis (OPLS-DA). (B) Score plots analyzed by GC-TOF-MS, UPLC-Q-TOF-MS, and Nanomate-LTQ-MS using SIMCA P+ (version 12.0, Umetrics, UMEÅ, Sweden). (C) Hepatic metabolites significantly altered (VIP >1.0 and p -value <0.05) by ezetimibe treatment from each OPLS-DA model. The significantly different hepatic metabolites were selected based on variable importance projection (VIP) values, and significance was tested by analysis of variance (ANOVA) between experimental groups. The relative level of each metabolite was normalized to that of the control group. (D) Correlation network between phenotype data and hepatic metabolites according to Pearson’s correlation coefficient (red line: r > 0.65 or blue line: r < −0.65) in ezetimibe-treated rat livers. (E) Combined ROC curves of potential hepatic biomarkers by ezetimibe treatment in OLETF rat livers. Abbreviations: AUC: area under the curve; CONT: control; EZ: ezetimibe; lysoPC: lysophosphatidylcholine; PC: phosphatidylcholine; PE: phosphatidylethanolamine; ROC: receiver operating characteristic; TCA: taurine-conjugated cholic acid; TDCA: taurine-conjugated deoxycholic acid.

Journal: Frontiers in Pharmacology

Article Title: Ezetimibe, Niemann-Pick C1 like 1 inhibitor, modulates hepatic phospholipid metabolism to alleviate fat accumulation

doi: 10.3389/fphar.2024.1406493

Figure Lengend Snippet: Metabolomic and lipidomic analyses. (A, B) Principal component analysis (PCA) (A) and orthogonal partial least squares discriminant analysis (OPLS-DA). (B) Score plots analyzed by GC-TOF-MS, UPLC-Q-TOF-MS, and Nanomate-LTQ-MS using SIMCA P+ (version 12.0, Umetrics, UMEÅ, Sweden). (C) Hepatic metabolites significantly altered (VIP >1.0 and p -value <0.05) by ezetimibe treatment from each OPLS-DA model. The significantly different hepatic metabolites were selected based on variable importance projection (VIP) values, and significance was tested by analysis of variance (ANOVA) between experimental groups. The relative level of each metabolite was normalized to that of the control group. (D) Correlation network between phenotype data and hepatic metabolites according to Pearson’s correlation coefficient (red line: r > 0.65 or blue line: r < −0.65) in ezetimibe-treated rat livers. (E) Combined ROC curves of potential hepatic biomarkers by ezetimibe treatment in OLETF rat livers. Abbreviations: AUC: area under the curve; CONT: control; EZ: ezetimibe; lysoPC: lysophosphatidylcholine; PC: phosphatidylcholine; PE: phosphatidylethanolamine; ROC: receiver operating characteristic; TCA: taurine-conjugated cholic acid; TDCA: taurine-conjugated deoxycholic acid.

Article Snippet: The ezetimibe stock solution was prepared in dimethylsulfoxide (DMSO; Sigma-Aldrich).

Techniques: Control

Effect of ezetimibe on hepatic phospholipid and lipid metabolism in OLETF rat liver. (A) Quantitative analysis of hepatic levels of total PC and PE, the ratio of PC to PE, and total lysoPC in rat liver. (B) Relative mRNA expression of genes related to phosphatidylcholine biosynthesis and remodeling in rat liver. (C) PLA 2 enzyme activity in rat liver ( n = 8 for each group). (D) Relative mRNA expression of CCTα, LPCAT3, or PEMT in HepG2 cells after siRNA transfection. (E–G) Quantitative analysis of intracellular TG amount in siRNA transfected HepG2 cells prior to ezetimibe treatment with or without 2 mM OA for 18 h ( n = 4 independent experiments). Relative mRNA expression of genes related to (H) de novo lipogenesis, and (I) fatty acid β-oxidation in rat liver ( n = 7 for each group). (J) PC-PLC enzyme activity in rat liver ( n = 8 for each group). Data are expressed as the mean ± S.E.M. * p < 0.05, ** p < 0.01, *** p < 0.001 vs . control, by Student’s t-test. Abbreviations: Acc1α : acetyl-CoA carboxylase 1α; Acadl : acyl-CoA dehydrogenase long chain; Acadm : acyl-CoA dehydrogenase medium chain; Acox1 : acyl-CoA oxidase 1; Acsl1 : long-chain acyl-coenzyme A synthetase 1; Cctα: CTP:phosphpocholine cytidylyltransferase alpha; Cpt1-α : carnitine palmitoyltransferase 1α; Dgat : diacylglycerol acyltransferase; Elovl5 : elongation of very long chain fatty acids protein 5; EZ: ezetimibe; Fads2 : fatty acid desaturase 2; Fasn : fatty acid synthase; Fatp5 : fatty acid transport protein 5; L-Fabp : liver fatty acid-binding protein; Lpcat : lysophosphatidylcholine acyltransferase; lysoPC: lysophosphatidylcholine; PC: phosphatidylcholine; PE: phosphatidylethanolamine; Pemt : phosphatidylethanolamine N-methyl-transferase; Pla2g4α: phospholipase A2 Group IVA; PC-PLC: PC-specific phospholipase C; Ppar-α : peroxisome proliferator-activated receptor-α; OA: oleic acid; Scd1 : stearoyl-CoA desaturase-1; Srebp1c : sterol regulatory element-binding protein 1c; TG: triglyceride.

Journal: Frontiers in Pharmacology

Article Title: Ezetimibe, Niemann-Pick C1 like 1 inhibitor, modulates hepatic phospholipid metabolism to alleviate fat accumulation

doi: 10.3389/fphar.2024.1406493

Figure Lengend Snippet: Effect of ezetimibe on hepatic phospholipid and lipid metabolism in OLETF rat liver. (A) Quantitative analysis of hepatic levels of total PC and PE, the ratio of PC to PE, and total lysoPC in rat liver. (B) Relative mRNA expression of genes related to phosphatidylcholine biosynthesis and remodeling in rat liver. (C) PLA 2 enzyme activity in rat liver ( n = 8 for each group). (D) Relative mRNA expression of CCTα, LPCAT3, or PEMT in HepG2 cells after siRNA transfection. (E–G) Quantitative analysis of intracellular TG amount in siRNA transfected HepG2 cells prior to ezetimibe treatment with or without 2 mM OA for 18 h ( n = 4 independent experiments). Relative mRNA expression of genes related to (H) de novo lipogenesis, and (I) fatty acid β-oxidation in rat liver ( n = 7 for each group). (J) PC-PLC enzyme activity in rat liver ( n = 8 for each group). Data are expressed as the mean ± S.E.M. * p < 0.05, ** p < 0.01, *** p < 0.001 vs . control, by Student’s t-test. Abbreviations: Acc1α : acetyl-CoA carboxylase 1α; Acadl : acyl-CoA dehydrogenase long chain; Acadm : acyl-CoA dehydrogenase medium chain; Acox1 : acyl-CoA oxidase 1; Acsl1 : long-chain acyl-coenzyme A synthetase 1; Cctα: CTP:phosphpocholine cytidylyltransferase alpha; Cpt1-α : carnitine palmitoyltransferase 1α; Dgat : diacylglycerol acyltransferase; Elovl5 : elongation of very long chain fatty acids protein 5; EZ: ezetimibe; Fads2 : fatty acid desaturase 2; Fasn : fatty acid synthase; Fatp5 : fatty acid transport protein 5; L-Fabp : liver fatty acid-binding protein; Lpcat : lysophosphatidylcholine acyltransferase; lysoPC: lysophosphatidylcholine; PC: phosphatidylcholine; PE: phosphatidylethanolamine; Pemt : phosphatidylethanolamine N-methyl-transferase; Pla2g4α: phospholipase A2 Group IVA; PC-PLC: PC-specific phospholipase C; Ppar-α : peroxisome proliferator-activated receptor-α; OA: oleic acid; Scd1 : stearoyl-CoA desaturase-1; Srebp1c : sterol regulatory element-binding protein 1c; TG: triglyceride.

Article Snippet: The ezetimibe stock solution was prepared in dimethylsulfoxide (DMSO; Sigma-Aldrich).

Techniques: Expressing, Activity Assay, Transfection, Control, Binding Assay

The proposed hepatic metabolic pathway and altered gene expression by treatment with ezetimibe (white arrow) in a rat model of obesity and type 2 diabetes. Abbreviations: ACSL1 : long-chain acyl-coenzyme A synthetase 1; CCTα: CTP:phosphpocholine cytidylyltransferase alpha; DGAT : diacylglycerol acyltransferase; ELOVL5 : elongation of very long chain fatty acids protein 5; FADS2 : fatty acid desaturase 2; FATP5 : fatty acid transport protein 5; L-FABP : liver fatty acid-binding protein; LPCAT : lysophosphatidylcholine acyltransferase; PC: phosphatidylcholine; PE: phosphatidylethanolamine; PEMT : phosphatidylethanolamine N-methyl-transferase; PLA 2 : phospholipase A 2 ; PC-PLC: PC-specific phospholipase C.

Journal: Frontiers in Pharmacology

Article Title: Ezetimibe, Niemann-Pick C1 like 1 inhibitor, modulates hepatic phospholipid metabolism to alleviate fat accumulation

doi: 10.3389/fphar.2024.1406493

Figure Lengend Snippet: The proposed hepatic metabolic pathway and altered gene expression by treatment with ezetimibe (white arrow) in a rat model of obesity and type 2 diabetes. Abbreviations: ACSL1 : long-chain acyl-coenzyme A synthetase 1; CCTα: CTP:phosphpocholine cytidylyltransferase alpha; DGAT : diacylglycerol acyltransferase; ELOVL5 : elongation of very long chain fatty acids protein 5; FADS2 : fatty acid desaturase 2; FATP5 : fatty acid transport protein 5; L-FABP : liver fatty acid-binding protein; LPCAT : lysophosphatidylcholine acyltransferase; PC: phosphatidylcholine; PE: phosphatidylethanolamine; PEMT : phosphatidylethanolamine N-methyl-transferase; PLA 2 : phospholipase A 2 ; PC-PLC: PC-specific phospholipase C.

Article Snippet: The ezetimibe stock solution was prepared in dimethylsulfoxide (DMSO; Sigma-Aldrich).

Techniques: Expressing, Binding Assay

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