resolvin d2  (MedChemExpress)

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 upregulates the NRF2 signaling cascade in TNFɑ-induced JEG-3 cells. For cotreatment of TNFɑ + RvD2 (TR) groups, cells were pretreated with RvD2 for 16 h, followed by TNFɑ treatment for an additional 5 or 10 h (16 + 5 h or 16 + 10 h), resulting in total treatment durations of 21 and 26 h, respectively. For vehicle (V) or RvD2 (R) treatments, cells were treated for a total of 21 or 26 h. Cells treated with TNFɑ (T) were exposed for either 5 or 10 h. (A) Immunoblot analysis of NRF2 in 16 + 5 h and 16 + 10 h treatment strategies. The values below the immunoblot represent band intensity ratio of nNRF2/HDAC1. The same blot was used in . (B–G) Relative mRNA expression of 16 + 5 h treatment strategy of kelch-like ECH-associated protein 1 (KEAP1), hemoxygenase 1 (HOXO1), glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase modifier subunit (GCLM), NADPH quinone oxidoreductase 1 (NQO1) in trophoblasts; n = 3 per group. (H) Reduced glutathione was measured with the pretreatment of RvD2 (100 nM) for 16 h followed by a 1 h treatment of TNFɑ (100 ng/mL); n = 5–7 per group. Data presented as mean ± SEM; *p < 0.05 and **p < 0.01 compared against each treatment.

Article Snippet: JEG-3 cells were cultured to 70%–80% confluency on MatTek 35 mm glass-bottom dishes (P35G-1.5-20-C) and pre-treated with Vehicle, RvD2, or Mitoquinone mesylate (MitoQ, TargetMOI Chemicals #845959-50-4) at 16 h prior to imaging.

Techniques: Western Blot, Expressing

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 increases NRF2 expression in the presence of TNFα after 24 h. JEG-3 cells were treated with 100 nM RvD2, 50 ng/mL TNFα, or a combination of RvD2 + TNFα for 24 h. (A) Immunofluorescence images: blue represents DAPI (nuclei), and green represents NRF2. Teal areas within the DAPI-stained regions in the merged and zoomed-in images indicate increased nuclear colocalization of NRF2 with cotreatment of TNFα and RvD2. (B) Quantification of relative intensity of NRF2 expression from images converted to binary format, compared to DAPI. At least 100 cells per treatment condition were analyzed for the relative intensity ratio of NRF2:DAPI. Data are presented as mean ± SEM; n = 4–5 per group; *p < 0.05, **p < 0.01, ***p < 0.001, compared to each treatment.

Article Snippet: JEG-3 cells were cultured to 70%–80% confluency on MatTek 35 mm glass-bottom dishes (P35G-1.5-20-C) and pre-treated with Vehicle, RvD2, or Mitoquinone mesylate (MitoQ, TargetMOI Chemicals #845959-50-4) at 16 h prior to imaging.

Techniques: Expressing, Immunofluorescence, Staining

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 mitigates TNFα-induced mitochondrial ROS in trophoblast cells. Relative ROS intensity was measured using MitoSOX fluorescent dye. (A) Representative live-cell confocal microscopy images of JEG-3 cells pretreated for 16 h with 100 nM RvD2, 10 µM Mitoquinone mesylate (MitoQ) as a positive control, or Vehicle. After pretreatment, cells were exposed to 100 ng/mL TNFα “ + T NFα” or medium “ +Medium ” for 15 min during live-cell confocal imaging. Images were taken immediately after treatment and 15 min post-treatment following the partial medium replacement with either warm TNFα or medium. The intensity ratios of ROS were calculated at baseline/before “B” and post-treatment/after “A” at 1, 5, 10, and 15-min intervals, with a baseline ratio value set to 1. (B) A line graph showing ROS intensity over time for each treatment group, compared to the Vehicle controls from the same day, and comparing the before and after images for each group. (C) The accompanying bar chart illustrates the area under the curve (AUC) in arbitrary units (AU), where Vehicle is set to one. Data are presented as mean ± SEM; n = 3–4 per group; ****p < 0.0001, compared against MitoQ, TNFɑ, RvD2, and TNFɑ + RvD2.

Article Snippet: JEG-3 cells were cultured to 70%–80% confluency on MatTek 35 mm glass-bottom dishes (P35G-1.5-20-C) and pre-treated with Vehicle, RvD2, or Mitoquinone mesylate (MitoQ, TargetMOI Chemicals #845959-50-4) at 16 h prior to imaging.

Techniques: Confocal Microscopy, Positive Control, Imaging

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: Pretreatment of RvD2 reduces TNFα-induced oxygen consumption rates (OCR) without altering electron transport chain (ETC) proteins. Bioenergetic Seahorse™ analysis of JEG-3 cells pretreated for 16 h with Vehicle or 100 nM RvD2, followed by a 5-h treatment of 100 ng/mL TNFα. (A) OCR levels were measured during injections of Oligomycin (Oligo; 1 μM), Carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP; 1 μM), and Rotenone/Antimycin A (R/A; 0.5 μM). (B) Area under the curve (AUC) in arbitrary units (AU). (C–H) Comparison of OCR values for basal, maximal, and spare respiratory capacity, proton leak, ATP production, and non-mitochondrial respiration between groups, n = 3–6 per group. (I) Immunoblot representative images showing mitochondrial protein fractions for total ETC complex proteins from JEG-3 cells pretreated with Vehicle (V) or 100 nM RvD2 (R 100 ), followed by a 5-h treatment with 50-100 ng/mL TNFα (T 50 or T 100 ). Data are presented as mean ± SEM; *p < 0.05, **p < 0.01, and ***p < 0.001.

Article Snippet: JEG-3 cells were cultured to 70%–80% confluency on MatTek 35 mm glass-bottom dishes (P35G-1.5-20-C) and pre-treated with Vehicle, RvD2, or Mitoquinone mesylate (MitoQ, TargetMOI Chemicals #845959-50-4) at 16 h prior to imaging.

Techniques: Comparison, Western Blot

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 improves mitochondrial function in a TNFɑ-induced environment in trophoblasts. JEG-3 cells were pretreated with 100 nM of RvD2 for 16 h, followed by a 1-hour exposure to 100 ng/mL of TNFɑ. (A) Representative dot plot analysis of cell populations stained with MitoTracker™ Green and MitoTracker™ Red CMXRos using flow cytometry. (B) Functional mitochondria were identified as MitoTracker™ Red high (+) and MitoTracker™ Green high (+) , denoted as “R+G+”. (C) Cells with dysfunctional mitochondria were classified as MitoTracker™ Red low (−) and MitoTracker™ Green high (+) , denoted as “R−G+”. (D) Representative flow cytometry median peak intensity graphs (events vs. MitoTracker™ Green fluorescence intensity and events vs. MitoTracker™ Red fluorescence intensity). Data presented as mean ± SEM; n = 4−5 per group; *p < 0.05.

Article Snippet: JEG-3 cells were cultured to 70%–80% confluency on MatTek 35 mm glass-bottom dishes (P35G-1.5-20-C) and pre-treated with Vehicle, RvD2, or Mitoquinone mesylate (MitoQ, TargetMOI Chemicals #845959-50-4) at 16 h prior to imaging.

Techniques: Staining, Flow Cytometry, Functional Assay, Fluorescence

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 stimulates mitochondrial biogenesis, increases mitochondrial content and improves migration. For cotreatment of TNFɑ + RvD2 (TR) groups, cells were pretreated with RvD2 for 16 h, followed by TNFɑ treatment for an additional 5 or 10 h (16 + 5 h or 16 + 10 h), resulting in total treatment durations of 21 and 26 h, respectively. For vehicle (V) or RvD2 (R) treatments, cells were treated for a total of 21 or 26 h. Cells treated with TNFɑ (T) were exposed for either 5 or 10 h. (A) Immunoblot representative of treatments. The values below the immunoblot represent band intensity ratio of PGC1ɑ/HDAC1. The same blot was used in . (B) RT-qPCR results for 16 + 5 h treatment strategy of PGC1α, (C) TFAM, and (D) Relative mitochondrial DNA (mtDNA) content was compared by taking the ratio of nuclear DNA to mtDNA relative mRNA expression; n = 3 per group. (E) MitoTracker™ Green relative fluorescence units (RFU) were measured using the 16 + 5 h treatment strategy. For the migration assay, cells were treated for 24 h with Vehicle, 100 nM of RvD2, 50 ng/mL TNFɑ, and RvD2 + TNFɑ; n = 6– 1 2 per group. (G) Migration bar chart (percentages, %) of various groups; n = 6–12. (F) Representative images of the scratch assay. Data are presented as mean ± SEM; *p < 0.05 and **p < 0.01.

Article Snippet: JEG-3 cells were cultured to 70%–80% confluency on MatTek 35 mm glass-bottom dishes (P35G-1.5-20-C) and pre-treated with Vehicle, RvD2, or Mitoquinone mesylate (MitoQ, TargetMOI Chemicals #845959-50-4) at 16 h prior to imaging.

Techniques: Migration, Western Blot, Quantitative RT-PCR, Expressing, Fluorescence, Wound Healing Assay

Journal: Cancers

Article Title: Effects of DHA Oral Supplementation on Plasma Resolvin D1 and D2 Levels in Naïve Breast Cancer Patients

doi: 10.3390/cancers17101694

Figure Lengend Snippet: Baseline (T0) plasma levels of resolvin D1 (panel ( A )) and resolvin D2 (panel ( B )) in breast cancer patients and controls. Data are expressed as median with 95% CI.

Article Snippet: Plasma levels of resolvins D1 and D2 were quantified using the available enzyme-linked immunosorbent assay (ELISA) kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL) and Human Resolvin D2 (RvD2) (Cat. No.: MBS051498, sensitivity 5.0 pg/mL), according to the manufacturer’s protocol.

Techniques: Clinical Proteomics

Journal: Cancers

Article Title: Effects of DHA Oral Supplementation on Plasma Resolvin D1 and D2 Levels in Naïve Breast Cancer Patients

doi: 10.3390/cancers17101694

Figure Lengend Snippet: Baseline (T0) plasma levels of resolvin D1 in breast cancer patients according to the type of presentation (sporadic, familial, and BRCA1/2-mutated) and in controls. Data are expressed as median with 95% CI. p -Values are obtained from post-hoc analysis.

Article Snippet: Plasma levels of resolvins D1 and D2 were quantified using the available enzyme-linked immunosorbent assay (ELISA) kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL) and Human Resolvin D2 (RvD2) (Cat. No.: MBS051498, sensitivity 5.0 pg/mL), according to the manufacturer’s protocol.

Techniques: Clinical Proteomics

Journal: Cancers

Article Title: Effects of DHA Oral Supplementation on Plasma Resolvin D1 and D2 Levels in Naïve Breast Cancer Patients

doi: 10.3390/cancers17101694

Figure Lengend Snippet: Change from baseline (T0) in plasma resolvin D1 and D2 levels after DHA supplementation (T1) in BRCA1/2-mutated (Panels ( A , B )) and familial (Panels ( C , D )) groups. Data are presented as median with IQR.

Article Snippet: Plasma levels of resolvins D1 and D2 were quantified using the available enzyme-linked immunosorbent assay (ELISA) kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL) and Human Resolvin D2 (RvD2) (Cat. No.: MBS051498, sensitivity 5.0 pg/mL), according to the manufacturer’s protocol.

Techniques: Clinical Proteomics

Journal: Cancers

Article Title: Effects of DHA Oral Supplementation on Plasma Resolvin D1 and D2 Levels in Naïve Breast Cancer Patients

doi: 10.3390/cancers17101694

Figure Lengend Snippet: Change of plasma resolvin D1 levels (Δ%T0-T1) in breast cancer patients (according to the type of presentation) and in controls. Data are expressed as median with 95% CI. p -values are obtained from post-hoc analysis.

Article Snippet: Plasma levels of resolvins D1 and D2 were quantified using the available enzyme-linked immunosorbent assay (ELISA) kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL) and Human Resolvin D2 (RvD2) (Cat. No.: MBS051498, sensitivity 5.0 pg/mL), according to the manufacturer’s protocol.

Techniques: Clinical Proteomics

Journal: Cancers

Article Title: Effects of DHA Oral Supplementation on Plasma Resolvin D1 and D2 Levels in Naïve Breast Cancer Patients

doi: 10.3390/cancers17101694

Figure Lengend Snippet: Change of plasma resolvin D2 levels (Δ%T0-T1) in breast cancer patients with high Ki67% (≥20) vs. low Ki67% (<20) levels. Data are expressed as median with IQR.

Article Snippet: Plasma levels of resolvins D1 and D2 were quantified using the available enzyme-linked immunosorbent assay (ELISA) kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL) and Human Resolvin D2 (RvD2) (Cat. No.: MBS051498, sensitivity 5.0 pg/mL), according to the manufacturer’s protocol.

Techniques: Clinical Proteomics

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 upregulates the NRF2 signaling cascade in TNFɑ-induced JEG-3 cells. For cotreatment of TNFɑ + RvD2 (TR) groups, cells were pretreated with RvD2 for 16 h, followed by TNFɑ treatment for an additional 5 or 10 h (16 + 5 h or 16 + 10 h), resulting in total treatment durations of 21 and 26 h, respectively. For vehicle (V) or RvD2 (R) treatments, cells were treated for a total of 21 or 26 h. Cells treated with TNFɑ (T) were exposed for either 5 or 10 h. (A) Immunoblot analysis of NRF2 in 16 + 5 h and 16 + 10 h treatment strategies. The values below the immunoblot represent band intensity ratio of nNRF2/HDAC1. The same blot was used in . (B–G) Relative mRNA expression of 16 + 5 h treatment strategy of kelch-like ECH-associated protein 1 (KEAP1), hemoxygenase 1 (HOXO1), glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase modifier subunit (GCLM), NADPH quinone oxidoreductase 1 (NQO1) in trophoblasts; n = 3 per group. (H) Reduced glutathione was measured with the pretreatment of RvD2 (100 nM) for 16 h followed by a 1 h treatment of TNFɑ (100 ng/mL); n = 5–7 per group. Data presented as mean ± SEM; *p < 0.05 and **p < 0.01 compared against each treatment.

Article Snippet: Resolvin D2 (RvD2, Cayman Chemical #10007279) was purchased from the manufacturer as 20 μg in 250 μL of 100% ethanol stored at −80°C.

Techniques: Western Blot, Expressing

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 increases NRF2 expression in the presence of TNFα after 24 h. JEG-3 cells were treated with 100 nM RvD2, 50 ng/mL TNFα, or a combination of RvD2 + TNFα for 24 h. (A) Immunofluorescence images: blue represents DAPI (nuclei), and green represents NRF2. Teal areas within the DAPI-stained regions in the merged and zoomed-in images indicate increased nuclear colocalization of NRF2 with cotreatment of TNFα and RvD2. (B) Quantification of relative intensity of NRF2 expression from images converted to binary format, compared to DAPI. At least 100 cells per treatment condition were analyzed for the relative intensity ratio of NRF2:DAPI. Data are presented as mean ± SEM; n = 4–5 per group; *p < 0.05, **p < 0.01, ***p < 0.001, compared to each treatment.

Article Snippet: Resolvin D2 (RvD2, Cayman Chemical #10007279) was purchased from the manufacturer as 20 μg in 250 μL of 100% ethanol stored at −80°C.

Techniques: Expressing, Immunofluorescence, Staining

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 mitigates TNFα-induced mitochondrial ROS in trophoblast cells. Relative ROS intensity was measured using MitoSOX fluorescent dye. (A) Representative live-cell confocal microscopy images of JEG-3 cells pretreated for 16 h with 100 nM RvD2, 10 µM Mitoquinone mesylate (MitoQ) as a positive control, or Vehicle. After pretreatment, cells were exposed to 100 ng/mL TNFα “ + T NFα” or medium “ +Medium ” for 15 min during live-cell confocal imaging. Images were taken immediately after treatment and 15 min post-treatment following the partial medium replacement with either warm TNFα or medium. The intensity ratios of ROS were calculated at baseline/before “B” and post-treatment/after “A” at 1, 5, 10, and 15-min intervals, with a baseline ratio value set to 1. (B) A line graph showing ROS intensity over time for each treatment group, compared to the Vehicle controls from the same day, and comparing the before and after images for each group. (C) The accompanying bar chart illustrates the area under the curve (AUC) in arbitrary units (AU), where Vehicle is set to one. Data are presented as mean ± SEM; n = 3–4 per group; ****p < 0.0001, compared against MitoQ, TNFɑ, RvD2, and TNFɑ + RvD2.

Article Snippet: Resolvin D2 (RvD2, Cayman Chemical #10007279) was purchased from the manufacturer as 20 μg in 250 μL of 100% ethanol stored at −80°C.

Techniques: Confocal Microscopy, Positive Control, Imaging

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: Pretreatment of RvD2 reduces TNFα-induced oxygen consumption rates (OCR) without altering electron transport chain (ETC) proteins. Bioenergetic Seahorse™ analysis of JEG-3 cells pretreated for 16 h with Vehicle or 100 nM RvD2, followed by a 5-h treatment of 100 ng/mL TNFα. (A) OCR levels were measured during injections of Oligomycin (Oligo; 1 μM), Carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP; 1 μM), and Rotenone/Antimycin A (R/A; 0.5 μM). (B) Area under the curve (AUC) in arbitrary units (AU). (C–H) Comparison of OCR values for basal, maximal, and spare respiratory capacity, proton leak, ATP production, and non-mitochondrial respiration between groups, n = 3–6 per group. (I) Immunoblot representative images showing mitochondrial protein fractions for total ETC complex proteins from JEG-3 cells pretreated with Vehicle (V) or 100 nM RvD2 (R 100 ), followed by a 5-h treatment with 50-100 ng/mL TNFα (T 50 or T 100 ). Data are presented as mean ± SEM; *p < 0.05, **p < 0.01, and ***p < 0.001.

Article Snippet: Resolvin D2 (RvD2, Cayman Chemical #10007279) was purchased from the manufacturer as 20 μg in 250 μL of 100% ethanol stored at −80°C.

Techniques: Comparison, Western Blot

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 improves mitochondrial function in a TNFɑ-induced environment in trophoblasts. JEG-3 cells were pretreated with 100 nM of RvD2 for 16 h, followed by a 1-hour exposure to 100 ng/mL of TNFɑ. (A) Representative dot plot analysis of cell populations stained with MitoTracker™ Green and MitoTracker™ Red CMXRos using flow cytometry. (B) Functional mitochondria were identified as MitoTracker™ Red high (+) and MitoTracker™ Green high (+) , denoted as “R+G+”. (C) Cells with dysfunctional mitochondria were classified as MitoTracker™ Red low (−) and MitoTracker™ Green high (+) , denoted as “R−G+”. (D) Representative flow cytometry median peak intensity graphs (events vs. MitoTracker™ Green fluorescence intensity and events vs. MitoTracker™ Red fluorescence intensity). Data presented as mean ± SEM; n = 4−5 per group; *p < 0.05.

Article Snippet: Resolvin D2 (RvD2, Cayman Chemical #10007279) was purchased from the manufacturer as 20 μg in 250 μL of 100% ethanol stored at −80°C.

Techniques: Staining, Flow Cytometry, Functional Assay, Fluorescence

Journal: Frontiers in Physiology

Article Title: RvD2 mitigates TNFɑ-Induced mitochondrial reactive oxygen species through NRF2 signaling in placental trophoblasts

doi: 10.3389/fphys.2025.1547940

Figure Lengend Snippet: RvD2 stimulates mitochondrial biogenesis, increases mitochondrial content and improves migration. For cotreatment of TNFɑ + RvD2 (TR) groups, cells were pretreated with RvD2 for 16 h, followed by TNFɑ treatment for an additional 5 or 10 h (16 + 5 h or 16 + 10 h), resulting in total treatment durations of 21 and 26 h, respectively. For vehicle (V) or RvD2 (R) treatments, cells were treated for a total of 21 or 26 h. Cells treated with TNFɑ (T) were exposed for either 5 or 10 h. (A) Immunoblot representative of treatments. The values below the immunoblot represent band intensity ratio of PGC1ɑ/HDAC1. The same blot was used in . (B) RT-qPCR results for 16 + 5 h treatment strategy of PGC1α, (C) TFAM, and (D) Relative mitochondrial DNA (mtDNA) content was compared by taking the ratio of nuclear DNA to mtDNA relative mRNA expression; n = 3 per group. (E) MitoTracker™ Green relative fluorescence units (RFU) were measured using the 16 + 5 h treatment strategy. For the migration assay, cells were treated for 24 h with Vehicle, 100 nM of RvD2, 50 ng/mL TNFɑ, and RvD2 + TNFɑ; n = 6– 1 2 per group. (G) Migration bar chart (percentages, %) of various groups; n = 6–12. (F) Representative images of the scratch assay. Data are presented as mean ± SEM; *p < 0.05 and **p < 0.01.

Article Snippet: Resolvin D2 (RvD2, Cayman Chemical #10007279) was purchased from the manufacturer as 20 μg in 250 μL of 100% ethanol stored at −80°C.

Techniques: Migration, Western Blot, Quantitative RT-PCR, Expressing, Fluorescence, Wound Healing Assay

Journal: Lipids in Health and Disease

Article Title: Assessment of plasma resolvin levels in women with breast cancer and their associations with disease presentation and immunohistochemical characteristics

doi: 10.1186/s12944-024-02386-5

Figure Lengend Snippet: Differences in plasma resolvin levels between patients with breast cancer and controls. The data revealed higher levels of resolvin D1 in breast cancer patients than in controls ( p = 0.015) (panel A). No differences were observed in resolvin D2, D3 or E1 levels between cancer patients and controls (panel B, C). Data are expressed as pg/ml and are presented as the median (95% CI). * p < 0.05

Article Snippet: All samples were analyzed via the commercially available ELISA kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL); Human Resolvin D2 (RvD2) (Cat. No: MBS051498, sensitivity 5.0 pg/mL); Human Resolvin D3 (RvD3) (Cat. No: MBS056544, sensitivity 2.0 pg/mL); and Resolvin E1 (RvE1) (Cat. No: MBS025958, sensitivity 5.0 pg/mL), in accordance with the manufacturer’s instructions reporting high sensitivity and excellent specificity ( https://www.mybiosource.com ).

Techniques: Clinical Proteomics

Journal: Lipids in Health and Disease

Article Title: Assessment of plasma resolvin levels in women with breast cancer and their associations with disease presentation and immunohistochemical characteristics

doi: 10.1186/s12944-024-02386-5

Figure Lengend Snippet: Linear correlations between plasma resolvin levels in breast cancer patients

Article Snippet: All samples were analyzed via the commercially available ELISA kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL); Human Resolvin D2 (RvD2) (Cat. No: MBS051498, sensitivity 5.0 pg/mL); Human Resolvin D3 (RvD3) (Cat. No: MBS056544, sensitivity 2.0 pg/mL); and Resolvin E1 (RvE1) (Cat. No: MBS025958, sensitivity 5.0 pg/mL), in accordance with the manufacturer’s instructions reporting high sensitivity and excellent specificity ( https://www.mybiosource.com ).

Techniques: Clinical Proteomics

Journal: Lipids in Health and Disease

Article Title: Assessment of plasma resolvin levels in women with breast cancer and their associations with disease presentation and immunohistochemical characteristics

doi: 10.1186/s12944-024-02386-5

Figure Lengend Snippet: Differences in plasma resolvin levels in the cancer group according to the form of presentation (sporadic, familiar and BRCA1/2 mutated groups). The data revealed lower levels of resolvin D1 in BRCA1/2-mutated patients than in the familiar and sporadic patients ( p = 0.031 and p = 0.020, respectively) (panel A). The data revealed lower levels of resolvin D3 in BRCA1/2-mutated patients than in the familiar and sporadic patients ( p = 0.031 and p = 0.013, respectively) (panel C). No difference was observed in the resolvins D2 and E1 levels among the three groups (panel B, D). Data are expressed as pg/ml and are presented as the median (95% CI). * p < 0.05

Article Snippet: All samples were analyzed via the commercially available ELISA kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL); Human Resolvin D2 (RvD2) (Cat. No: MBS051498, sensitivity 5.0 pg/mL); Human Resolvin D3 (RvD3) (Cat. No: MBS056544, sensitivity 2.0 pg/mL); and Resolvin E1 (RvE1) (Cat. No: MBS025958, sensitivity 5.0 pg/mL), in accordance with the manufacturer’s instructions reporting high sensitivity and excellent specificity ( https://www.mybiosource.com ).

Techniques: Clinical Proteomics

Journal: Lipids in Health and Disease

Article Title: Assessment of plasma resolvin levels in women with breast cancer and their associations with disease presentation and immunohistochemical characteristics

doi: 10.1186/s12944-024-02386-5

Figure Lengend Snippet: Differences in plasma resolvin levels between the sporadic plus familiar group and the BRCA1/2 mutated patient group. The data revealed lower levels of resolvin D1 and resolvin D3 in BRCA1/2-mutated patients than in the familiar plus sporadic patients ( p = 0.014 and p = 0.010, respectively) (panels A, C). Resolvin D2 and E1 levels tended to be lower in the BRCA1/2-mutated group than in the sporadic plus familiar group ( p = 0.051 and p = 0.062, respectively). Data are expressed as pg/ml and are presented as the median (95% CI). * p < 0.05

Article Snippet: All samples were analyzed via the commercially available ELISA kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL); Human Resolvin D2 (RvD2) (Cat. No: MBS051498, sensitivity 5.0 pg/mL); Human Resolvin D3 (RvD3) (Cat. No: MBS056544, sensitivity 2.0 pg/mL); and Resolvin E1 (RvE1) (Cat. No: MBS025958, sensitivity 5.0 pg/mL), in accordance with the manufacturer’s instructions reporting high sensitivity and excellent specificity ( https://www.mybiosource.com ).

Techniques: Clinical Proteomics

Journal: Lipids in Health and Disease

Article Title: Assessment of plasma resolvin levels in women with breast cancer and their associations with disease presentation and immunohistochemical characteristics

doi: 10.1186/s12944-024-02386-5

Figure Lengend Snippet: Differences in plasma resolvin D1 levels between triple-negative and nontriple-negative breast cancer patients. The data revealed lower levels of resolvin D1 in triple-negative patients than in non-triple-negative patients ( p = 0.023). Data are expressed as pg/ml and are presented as the median (95% CI). * p < 0.05

Article Snippet: All samples were analyzed via the commercially available ELISA kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL); Human Resolvin D2 (RvD2) (Cat. No: MBS051498, sensitivity 5.0 pg/mL); Human Resolvin D3 (RvD3) (Cat. No: MBS056544, sensitivity 2.0 pg/mL); and Resolvin E1 (RvE1) (Cat. No: MBS025958, sensitivity 5.0 pg/mL), in accordance with the manufacturer’s instructions reporting high sensitivity and excellent specificity ( https://www.mybiosource.com ).

Techniques: Clinical Proteomics

Journal: Lipids in Health and Disease

Article Title: Assessment of plasma resolvin levels in women with breast cancer and their associations with disease presentation and immunohistochemical characteristics

doi: 10.1186/s12944-024-02386-5

Figure Lengend Snippet: Differences in plasma resolvin D3 levels according to Ki-67% expression. The data revealed lower levels of resolvin D3 in breast cancer patients with high Ki-67 expression (≥ 20%) than in those with low Ki-67 expression ( p = 0.034). Data are expressed as pg/ml and are presented as the median (95% CI). * p < 0.05

Article Snippet: All samples were analyzed via the commercially available ELISA kits (Mybiosource, Inc., San Diego, CA, USA): Human Resolvin D1 (RvD1) (Cat. No: MBS053145, sensitivity 5.0 pg/mL); Human Resolvin D2 (RvD2) (Cat. No: MBS051498, sensitivity 5.0 pg/mL); Human Resolvin D3 (RvD3) (Cat. No: MBS056544, sensitivity 2.0 pg/mL); and Resolvin E1 (RvE1) (Cat. No: MBS025958, sensitivity 5.0 pg/mL), in accordance with the manufacturer’s instructions reporting high sensitivity and excellent specificity ( https://www.mybiosource.com ).

Techniques: Clinical Proteomics, Expressing

Journal: Frontiers in Immunology

Article Title: Disrupted balance between pro-inflammatory lipid mediators and anti-inflammatory specialized pro-resolving mediators is linked to hyperinflammation in patients with alcoholic hepatitis

doi: 10.3389/fimmu.2024.1377236

Figure Lengend Snippet: Dysregulated lipid mediators from the AA pathway in AH patients. (A) Simplified schematic representation of the AA metabolic pathway. Key biosynthetic enzymes are shown next to arrows, lipid intermediators in box, and proinflammatory lipid mediators in red and anti-inflammatory lipid in blue. (B–F) Scatter plots showing plasma levels of LTB4 (B, C) , PGD2 (D) , LXA4 (E) , and LTB4/LXA4 ratio (F) in healthy controls (HC), patients with alcoholic hepatitis (AH), and heavy drinking controls (HDC). Concentrations were measured by LC-MS/MS (B; open symbols) or ELISA (C-E; filled symbols). Kruskal-Wallis test with Dunn’s correction for pairwise comparison among AH, HDC, and HC. * p < 0.05, ** p < 0.01, *** p < 0.001. ns, not significant.

Article Snippet: Plasma levels of PGD2, PGE2, LTB4, LXA4, RvE1, RvD2, and MaR1 were quantified using the Prostaglandin D2 ELISA Kit (Cayman Chemical, Ann Arbor, MI), Prostaglandin E2 ELISA Kit (Cayman Chemical, Ann Arbor, MI), LTB4 Parameter Assay Kit (R&D Systems, Minneapolis, MN), Lipoxin A4 ELISA Kit (Neogen, Lexington, KY), Human Resolvin E1 ELISA Kit (MBS025958, MyBioSource, San Diego, CA), Resolvin D2 ELISA Kit (Cayman Chemical, Ann Arbor, MI), and Maresin 1 ELISA Kit (Cayman Chemical, Ann Arbor, MI), respectively.

Techniques: Clinical Proteomics, Liquid Chromatography with Mass Spectroscopy, Enzyme-linked Immunosorbent Assay, Comparison

Journal: Frontiers in Immunology

Article Title: Disrupted balance between pro-inflammatory lipid mediators and anti-inflammatory specialized pro-resolving mediators is linked to hyperinflammation in patients with alcoholic hepatitis

doi: 10.3389/fimmu.2024.1377236

Figure Lengend Snippet: Dysregulated RVE1 and its precursor 18-HEPE from the EPA pathway in AH patients. (A) Simplified schematic representation of the EPA metabolic pathway. Key biosynthetic enzymes are shown next to arrows, lipid intermediator in box, and anti-inflammatory SPMs in blue. (B, C) Scatter plots showing plasma levels of 18-HEPE (B) and RVE1 (C) in healthy controls (HC), patients with alcoholic hepatitis (AH), and heavy drinking controls (HDC). Concentrations were measured by LC-MS/MS (B; open symbols) or ELISA (C; filled symbols). Kruskal-Wallis test with Dunn’s correction for pairwise comparison among AH, HDC, and HC. ** p < 0.01, *** p < 0.001. ns, not significant.

Article Snippet: Plasma levels of PGD2, PGE2, LTB4, LXA4, RvE1, RvD2, and MaR1 were quantified using the Prostaglandin D2 ELISA Kit (Cayman Chemical, Ann Arbor, MI), Prostaglandin E2 ELISA Kit (Cayman Chemical, Ann Arbor, MI), LTB4 Parameter Assay Kit (R&D Systems, Minneapolis, MN), Lipoxin A4 ELISA Kit (Neogen, Lexington, KY), Human Resolvin E1 ELISA Kit (MBS025958, MyBioSource, San Diego, CA), Resolvin D2 ELISA Kit (Cayman Chemical, Ann Arbor, MI), and Maresin 1 ELISA Kit (Cayman Chemical, Ann Arbor, MI), respectively.

Techniques: Clinical Proteomics, Liquid Chromatography with Mass Spectroscopy, Enzyme-linked Immunosorbent Assay, Comparison

Journal: Journal of Lipid Research

Article Title: Resolvin D2/GPR 18 axis ameliorates pressure overload-induced heart failure by inhibiting pro-inflammatory macrophage polarization

doi: 10.1016/j.jlr.2024.100679

Figure Lengend Snippet: RvD2 ameliorated cardiac dysfunction and remodeling in TAC mice. A: schematic diagram depicting the experimental strategy for TAC models. B: the serum levels of RvD2 (n = 6 in each group). C–F: echocardiographic parameters for each group (n = 6 in each group). G–H: representative WGA staining and corresponding quantification showing cardiomyocyte size (n = 6 in each group). I–J: the ratio of heart weight to body weight or tibial length (n = 6 in each group). K–N: mRNA levels of NPPA, NPPB, MYH7, MYH6 (n = 6 in each group). O–P: representative Masson staining and corresponding quantification showing cardiac fibrosis (n = 6 in each group). Q: mRNA levels of COL1, COL3, TGF-β, CTGF, MMP2, MMP9 (n = 6 in each group). Values represent the mean ± SD. ∗ indicated P < 0.05, ∗∗ indicated P < 0.01, ∗∗∗ indicated P < 0.001, ns indicated no significant difference. BW, body weight; COL1, collagen 1; COL3, collagen 3; CTGF, connective tissue growth factor; EF, ejection fraction; FS, fractional shortening; HW, heart weight; LVIDd, left ventricular internal diameter at end-diastole; LVIDs, left ventricular internal diameter at end-systole; MMP2, matrix metallopeptidase 2; MMP9, matrix metallopeptidase 9; MYH6, myosin heavy chain 6; MYH7, myosin heavy chain 7; NPPA, natriuretic peptide a; NPPB, natriuretic peptide b; RvD2, Resolvin D2; TGF-β, transforming growth factor beta; TL, tibial length.

Article Snippet: To investigate the role of NF-κB p65 in RvD2 treated proinflammatory BMDMs, an agonist CU-T12-9 (50μM, Topscience), was administrated 30 min before RvD2 treatment.

Techniques: Staining

Journal: Journal of Lipid Research

Article Title: Resolvin D2/GPR 18 axis ameliorates pressure overload-induced heart failure by inhibiting pro-inflammatory macrophage polarization

doi: 10.1016/j.jlr.2024.100679

Figure Lengend Snippet: G pr 18 deficiency blocked the protective effect of RvD2 on cardiac dysfunction and remodeling in TAC mice. A: schematic diagram depicting the experimental strategy for TAC models. B: the serum levels of RvD2 (n = 6 in each group). C–F: echocardiographic parameters for each group (n = 6 in each group). G–H: representative WGA staining and corresponding quantification showing cardiomyocyte size (n = 6 in each group). I–J: the ratio of heart weight to body weight or tibial length (n = 6 in each group). K–N: mRNA levels of NPPA, NPPB, MYH7, MYH6 (n = 6 in each group). O–P: representative Masson staining and corresponding quantification showing cardiac fibrosis (n = 6 in each group). Q: mRNA levels of COL1, COL3, TGF-β, CTGF, MMP2, MMP9 (n = 6 in each group). Values represent the mean ± SD. ∗ indicated P < 0.05, ∗∗ indicated P < 0.01, ∗∗∗ indicated P < 0.001, ns indicated no significant difference. RvD2, Resolvin D2; LVIDd, left ventricular internal diameter at end-diastole; LVIDs, left ventricular internal diameter at end-systole; EF, ejection fraction; FS, fractional shortening; HW, heart weight; BW, body weight; TL, tibial length; NPPA, natriuretic peptide a; NPPB, natriuretic peptide b; MYH7, myosin heavy chain 7; MYH6, myosin heavy chain 6; COL1, collagen 1; COL3, collagen 3; TGF-β, transforming growth factor beta; CTGF, connective tissue growth factor; MMP2, matrix metallopeptidase 2; MMP9, matrix metallopeptidase 9.

Article Snippet: To investigate the role of NF-κB p65 in RvD2 treated proinflammatory BMDMs, an agonist CU-T12-9 (50μM, Topscience), was administrated 30 min before RvD2 treatment.

Techniques: Staining

Journal: Journal of Lipid Research

Article Title: Resolvin D2/GPR 18 axis ameliorates pressure overload-induced heart failure by inhibiting pro-inflammatory macrophage polarization

doi: 10.1016/j.jlr.2024.100679

Figure Lengend Snippet: RvD2 ameliorated inflammatory responses and inhibited proinflammatory macrophage polarization in TAC mice. A–C were detected in mice 1 week after TAC surgery. A: mRNA levels of IL-1β, IL-6, TNF-α (n = 6 in each group). B: mRNA levels of CD80, CD86, iNOS (n = 6 in each group). C: representative flow cytometry images and corresponding quantification showing the ratio of Ly6C high macrophages (n = 6 in each group). (D–F) were detected in mice 4 weeks after TAC surgery. D: mRNA levels of IL-1β, IL-6, TNF-α (n = 6 in each group). E: mRNA levels of CD80, CD86, iNOS (n = 6 in each group). F: representative flow cytometry images and corresponding quantification showing the ratio of Ly6C high macrophages (n = 6 in each group). Values represent the mean ± SD. ∗ indicated P < 0.05, ∗∗ indicated P < 0.01, ∗∗∗ indicated P < 0.001, ns indicated no significant difference. RvD2, Resolvin D2; IL, interleukin; TNF-α, tumor necrosis factor α; iNOS, inducible nitric oxide synthase.

Article Snippet: To investigate the role of NF-κB p65 in RvD2 treated proinflammatory BMDMs, an agonist CU-T12-9 (50μM, Topscience), was administrated 30 min before RvD2 treatment.

Techniques: Flow Cytometry

Journal: Journal of Lipid Research

Article Title: Resolvin D2/GPR 18 axis ameliorates pressure overload-induced heart failure by inhibiting pro-inflammatory macrophage polarization

doi: 10.1016/j.jlr.2024.100679

Figure Lengend Snippet: Bone marrow transplantation from G pr 18 deficient mice into WT mice blocked the protective effect of RvD2 on cardiac dysfunction and remodeling in TAC mice. A: schematic diagram depicting the experimental strategy for TAC models. B–E: echocardiographic parameters for each group (n = 6 in each group). F–G: representative WGA staining and corresponding quantification showing cardiomyocyte size (n = 6 in each group). H–I: the ratio of heart weight to body weight or tibial length (n = 6 in each group). J–M: mRNA levels of NPPA, NPPB, MYH7, MYH6 (n = 6 in each group). N–O: representative Masson staining and corresponding quantification showing cardiac fibrosis (n = 6 in each group). P: mRNA levels of COL1, COL3, TGF-β, CTGF, MMP2, MMP9 (n = 6 in each group). Values represent the mean ± SD. ∗ indicated P < 0.05, ∗∗ indicated P < 0.01, ∗∗∗ indicated P < 0.001, ns indicated no significant difference. RvD2, Resolvin D2; LVIDd, left ventricular internal diameter at end-diastole; LVIDs, left ventricular internal diameter at end-systole; EF, ejection fraction; FS, fractional shortening; BM, bone morrow; HW, heart weight; BW, body weight; TL, tibial length; NPPA, natriuretic peptide a; NPPB, natriuretic peptide b; MYH7, myosin heavy chain 7; MYH6, myosin heavy chain 6; COL1, collagen 1; COL3, collagen 3; TGF-β, transforming growth factor beta; CTGF, connective tissue growth factor; MMP2, matrix metallopeptidase 2; MMP9, matrix metallopeptidase 9.

Article Snippet: To investigate the role of NF-κB p65 in RvD2 treated proinflammatory BMDMs, an agonist CU-T12-9 (50μM, Topscience), was administrated 30 min before RvD2 treatment.

Techniques: Transplantation Assay, Staining

Journal: Journal of Lipid Research

Article Title: Resolvin D2/GPR 18 axis ameliorates pressure overload-induced heart failure by inhibiting pro-inflammatory macrophage polarization

doi: 10.1016/j.jlr.2024.100679

Figure Lengend Snippet: G pr 18 deficiency blocked the effect of RvD2 on inflammatory responses and macrophage polarization in TAC mice. A-C were detected in WT and G pr 18 deficient mice. A: mRNA levels of IL-1β, IL-6, TNF-α (n = 6 in each group). B: mRNA levels of CD80, CD86, iNOS (n = 6 in each group). C: Representative flow cytometry images and corresponding quantification showing the ratio of Ly6C high macrophages (n = 6 in each group). (D–F) were detected in mice accepted bone marrow transplantation. D: mRNA levels of IL-1β, IL-6, TNF-α (n = 6 in each group). E: mRNA levels of CD80, CD86, iNOS (n = 6 in each group). F: representative flow cytometry images and corresponding quantification showing the ratio of Ly6C high macrophages (n = 6 in each group). Values represent the mean ± SD. ∗ indicated P < 0.05, ∗∗ indicated P < 0.01, ∗∗∗ indicated P < 0.001, ns indicated no significant difference. RvD2, Resolvin D2; IL, interleukin; TNF-α, tumor necrosis factor α; iNOS, inducible nitric oxide synthase; BM, bone morrow.

Article Snippet: To investigate the role of NF-κB p65 in RvD2 treated proinflammatory BMDMs, an agonist CU-T12-9 (50μM, Topscience), was administrated 30 min before RvD2 treatment.

Techniques: Flow Cytometry, Transplantation Assay

Journal: Journal of Lipid Research

Article Title: Resolvin D2/GPR 18 axis ameliorates pressure overload-induced heart failure by inhibiting pro-inflammatory macrophage polarization

doi: 10.1016/j.jlr.2024.100679

Figure Lengend Snippet: RvD2 ameliorated inflammatory responses and inhibited the proinflammatory macrophage polarization through its receptor GPR18 in BMDMs , A-C were detected in BMDMs isolated from WT mice. A: mRNA levels of IL-1β, IL-6, TNF-α (n = 6 in each group). B: mRNA levels of CD80, CD86, iNOS (n = 6 in each group). C: Representative flow cytometry images and corresponding quantification showing the ratio of Ly6C high macrophages (n = 4 in each group). (D–F) were detected in BMDMs isolated from WT and G pr 18 deficient mice. D: mRNA levels of IL-1β, IL-6, TNF-α (n = 6 in each group). E: mRNA levels of CD80, CD86, iNOS (n = 6 in each group). F: Representative flow cytometry images and corresponding quantification showing the ratio of Ly6C high macrophages (n = 4 in each group). Values represent the mean ± SD. ∗ indicated P < 0.05, ∗∗ indicated P < 0.01, ∗∗∗ indicated P < 0.001, ns indicated no significant difference. RvD2, Resolvin D2; IL, interleukin; TNF-α, tumor necrosis factor α; iNOS, inducible nitric oxide synthase; BMDM, bone morrow-derived macrophage.

Article Snippet: To investigate the role of NF-κB p65 in RvD2 treated proinflammatory BMDMs, an agonist CU-T12-9 (50μM, Topscience), was administrated 30 min before RvD2 treatment.

Techniques: Isolation, Flow Cytometry, Derivative Assay

Journal: Journal of Lipid Research

Article Title: Resolvin D2/GPR 18 axis ameliorates pressure overload-induced heart failure by inhibiting pro-inflammatory macrophage polarization

doi: 10.1016/j.jlr.2024.100679

Figure Lengend Snippet: RvD2 ameliorated inflammatory response and inhibited the proinflammatory macrophage polarization via STAT1 and NF-κB p65 pathways. (A–C) were detected in mice 1 week after TAC surgery. A–C: Representative immunoblots and corresponding quantification showing levels of P-STAT1, T-STAT1, P-P65, T-P65 (n = 6 in each group). (D–I) were detected in BMDMs isolated from WT mice. D–F: representative immunoblots and corresponding quantification showing levels of P-STAT1, T-STAT1, P-P65, T-P65 (n = 4 in each group). G: mRNA levels of IL-1β, IL-6, TNF-α (n = 6 in each group). H: mRNA levels of CD80, CD86, iNOS (n = 6 in each group). I: representative flow cytometry images and corresponding quantification showing the ratio of Ly6C high macrophages (n = 4 in each group). Values represent the mean ± SD. ∗ indicated P < 0.05, ∗∗ indicated P < 0.01, ∗∗∗ indicated P < 0.001, ns indicated no significant difference. RvD2, Resolvin D2; IL, interleukin; TNF-α, tumor necrosis factor α; iNOS, inducible nitric oxide synthase.

Article Snippet: To investigate the role of NF-κB p65 in RvD2 treated proinflammatory BMDMs, an agonist CU-T12-9 (50μM, Topscience), was administrated 30 min before RvD2 treatment.

Techniques: Western Blot, Isolation, Flow Cytometry