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MedChemExpress dgat1 inhibitor t863
TAG are synthesized in the ER through sequential enzymatic reactions of GPAT, LPAAT, PAP1, and <t>DGAT.</t> CE are generated by SOAT. Seipin facilitates the incorporation of neutral lipids into the growing LD core, which buds from the ER and become coated by perilipins (PLINs). Stored neutral lipids are mobilized through lipolysis mediated by ATGL, HSL, and MGL or degraded via lysosomal lipophagy. Released free fatty acids and cholesterol can be utilized for cellular metabolism, while cholesterol may also undergo ABCA1- and ABCG1-mediated efflux to ApoE-containing HDL-like particles. Alternatively, cholesterol can be converted by CH25H to 25-hydroxycholesterol (25-HC), which readily crosses cellular membranes for export.
Dgat1 Inhibitor T863, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress t863
The apoptosis rate of HT22 cells following treatment with lipid synthesis inhibitors and lipid droplet inhibitors using flow cytometry. (A, B) Apoptosis in HT22 cells (A) and MA (B) were assessed after 24 hours of treatment with Lipofectamine 2000 (2 µL), siPLIN5 (30 nM), <t>T863</t> (20 µM), and firsocostat (10 µM) ( n = 3 independent experiments). (C) Apoptosis was assessed by Annexin V-FITC/PI staining. HT22 cells were then subjected to OA treatment for 24 hours. Flow cytometry was used to measure cell apoptosis rates at varying OA concentrations ( n = 3 independent experiments). (D, E) Apoptosis rates in monocultured (D) and cocultured (E) HT22 cells were measured after 24 hours of treatment ( n = 3 independent experiments). (F, G) Apoptosis rates in monocultured (F) and cocultured (G) MA were measured after 24 hours of treatment ( n = 3 independent experiments). (H) After 24 hours of siRNA treatment, MA in each group were treated for an additional 24 hours according to their specific grouping. The total apoptosis rate of the cells was then measured ( n = 3 independent experiments). (I) Western blot analysis was conducted to assess the expression levels of PLIN5, caspase-1, and caspase-1 p20 in MA. (J) Quantitative analysis of apoptosis rates in cocultured astrocytes ( n = 3 independent experiments) (corresponding to H). (K, L) Quantitative analysis of PLIN5 (K) and caspase-1 p20 (L). Relative protein expression was normalized to β-actin ( n = 3 independent experiments) (corresponding to I). (M) Quantitative analysis of LDs ( n = 3 independent experiments) (corresponding to N). (N) After 24 hours of treatment, immunofluorescence was used to detect LDs in cocultured astrocytes. Scale bar: 20 µm (40× magnification). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 (one-way analysis of variance followed by Tukey’s post hoc test [A–G and J–M]). DAPI: 4′,6-Diamidino-2-phenylindole; LDs: lipid droplets; MA: mouse astrocyte; ns: not significant; OA: oleic acid; PI: propidium iodide.
T863, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress ld formation
The apoptosis rate of HT22 cells following treatment with lipid synthesis inhibitors and lipid droplet inhibitors using flow cytometry. (A, B) Apoptosis in HT22 cells (A) and MA (B) were assessed after 24 hours of treatment with Lipofectamine 2000 (2 µL), siPLIN5 (30 nM), <t>T863</t> (20 µM), and firsocostat (10 µM) ( n = 3 independent experiments). (C) Apoptosis was assessed by Annexin V-FITC/PI staining. HT22 cells were then subjected to OA treatment for 24 hours. Flow cytometry was used to measure cell apoptosis rates at varying OA concentrations ( n = 3 independent experiments). (D, E) Apoptosis rates in monocultured (D) and cocultured (E) HT22 cells were measured after 24 hours of treatment ( n = 3 independent experiments). (F, G) Apoptosis rates in monocultured (F) and cocultured (G) MA were measured after 24 hours of treatment ( n = 3 independent experiments). (H) After 24 hours of siRNA treatment, MA in each group were treated for an additional 24 hours according to their specific grouping. The total apoptosis rate of the cells was then measured ( n = 3 independent experiments). (I) Western blot analysis was conducted to assess the expression levels of PLIN5, caspase-1, and caspase-1 p20 in MA. (J) Quantitative analysis of apoptosis rates in cocultured astrocytes ( n = 3 independent experiments) (corresponding to H). (K, L) Quantitative analysis of PLIN5 (K) and caspase-1 p20 (L). Relative protein expression was normalized to β-actin ( n = 3 independent experiments) (corresponding to I). (M) Quantitative analysis of LDs ( n = 3 independent experiments) (corresponding to N). (N) After 24 hours of treatment, immunofluorescence was used to detect LDs in cocultured astrocytes. Scale bar: 20 µm (40× magnification). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 (one-way analysis of variance followed by Tukey’s post hoc test [A–G and J–M]). DAPI: 4′,6-Diamidino-2-phenylindole; LDs: lipid droplets; MA: mouse astrocyte; ns: not significant; OA: oleic acid; PI: propidium iodide.
Ld Formation, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
MedChemExpress hy10038 hy 32219
The apoptosis rate of HT22 cells following treatment with lipid synthesis inhibitors and lipid droplet inhibitors using flow cytometry. (A, B) Apoptosis in HT22 cells (A) and MA (B) were assessed after 24 hours of treatment with Lipofectamine 2000 (2 µL), siPLIN5 (30 nM), <t>T863</t> (20 µM), and firsocostat (10 µM) ( n = 3 independent experiments). (C) Apoptosis was assessed by Annexin V-FITC/PI staining. HT22 cells were then subjected to OA treatment for 24 hours. Flow cytometry was used to measure cell apoptosis rates at varying OA concentrations ( n = 3 independent experiments). (D, E) Apoptosis rates in monocultured (D) and cocultured (E) HT22 cells were measured after 24 hours of treatment ( n = 3 independent experiments). (F, G) Apoptosis rates in monocultured (F) and cocultured (G) MA were measured after 24 hours of treatment ( n = 3 independent experiments). (H) After 24 hours of siRNA treatment, MA in each group were treated for an additional 24 hours according to their specific grouping. The total apoptosis rate of the cells was then measured ( n = 3 independent experiments). (I) Western blot analysis was conducted to assess the expression levels of PLIN5, caspase-1, and caspase-1 p20 in MA. (J) Quantitative analysis of apoptosis rates in cocultured astrocytes ( n = 3 independent experiments) (corresponding to H). (K, L) Quantitative analysis of PLIN5 (K) and caspase-1 p20 (L). Relative protein expression was normalized to β-actin ( n = 3 independent experiments) (corresponding to I). (M) Quantitative analysis of LDs ( n = 3 independent experiments) (corresponding to N). (N) After 24 hours of treatment, immunofluorescence was used to detect LDs in cocultured astrocytes. Scale bar: 20 µm (40× magnification). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 (one-way analysis of variance followed by Tukey’s post hoc test [A–G and J–M]). DAPI: 4′,6-Diamidino-2-phenylindole; LDs: lipid droplets; MA: mouse astrocyte; ns: not significant; OA: oleic acid; PI: propidium iodide.
Hy10038 Hy 32219, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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TAG are synthesized in the ER through sequential enzymatic reactions of GPAT, LPAAT, PAP1, and DGAT. CE are generated by SOAT. Seipin facilitates the incorporation of neutral lipids into the growing LD core, which buds from the ER and become coated by perilipins (PLINs). Stored neutral lipids are mobilized through lipolysis mediated by ATGL, HSL, and MGL or degraded via lysosomal lipophagy. Released free fatty acids and cholesterol can be utilized for cellular metabolism, while cholesterol may also undergo ABCA1- and ABCG1-mediated efflux to ApoE-containing HDL-like particles. Alternatively, cholesterol can be converted by CH25H to 25-hydroxycholesterol (25-HC), which readily crosses cellular membranes for export.

Journal: bioRxiv

Article Title: Accumulation of Lipid Droplets in Microglia following Neonatal Brain Hypoxia-Ischemia

doi: 10.64898/2026.07.18.739219

Figure Lengend Snippet: TAG are synthesized in the ER through sequential enzymatic reactions of GPAT, LPAAT, PAP1, and DGAT. CE are generated by SOAT. Seipin facilitates the incorporation of neutral lipids into the growing LD core, which buds from the ER and become coated by perilipins (PLINs). Stored neutral lipids are mobilized through lipolysis mediated by ATGL, HSL, and MGL or degraded via lysosomal lipophagy. Released free fatty acids and cholesterol can be utilized for cellular metabolism, while cholesterol may also undergo ABCA1- and ABCG1-mediated efflux to ApoE-containing HDL-like particles. Alternatively, cholesterol can be converted by CH25H to 25-hydroxycholesterol (25-HC), which readily crosses cellular membranes for export.

Article Snippet: DGAT1 inhibitor T863 (Cat# HY-32219, MedChemiExpress LCC, Monmouth Junction, NJ), and DGAT2 inhibitor PF-06424439 (Cat# HY-108341A, MCE) were dissolved in DMSO and used at 30 μM and 40 μM, respectively.

Techniques: Synthesized, Generated

A). Representative images of PLIN2 (white) expression and Dextran uptake (green) in BV2 cells following DGAT inhibitor treatment. BV2 cells were treated with DGAT1 inhibitor T863 or DGAT2 inhibitor PF-06424439 (PF) or DMSO vehicle control under normoxic control or OGD condition. Scale bar = 20 µm. n = 3 per group. B). Representative flow cytometric histograms showing PLIN2 fluorescence intensity curves under different treatment conditions. Blank group cells received medium as no-treatment control. C). Percentage of PLIN2 + cells in BV2 cells under different treatment conditions. D). PLIN2 mean fluorescence intensity (MFI) in BV2 cells under different treatment conditions. E). Representative flow cytometric histograms showing Dextran 40 fluorescence intensity curves under different conditions. F). Percentage of Dextran 40 + cells in BV2 cells under different treatment conditions. G). Dextran 40 MFI under different treatment conditions. For flow cytometry, n = 6 per group; data are presented as mean ± SD; two-way ANOVA (OGD × drug) with Tukey’s multiple comparisons test; *p < 0.05, **p < 0.01, ***p < 0.001 vs. OGD and DMSO group; ### p < 0.001 vs. OGD + Blank group.

Journal: bioRxiv

Article Title: Accumulation of Lipid Droplets in Microglia following Neonatal Brain Hypoxia-Ischemia

doi: 10.64898/2026.07.18.739219

Figure Lengend Snippet: A). Representative images of PLIN2 (white) expression and Dextran uptake (green) in BV2 cells following DGAT inhibitor treatment. BV2 cells were treated with DGAT1 inhibitor T863 or DGAT2 inhibitor PF-06424439 (PF) or DMSO vehicle control under normoxic control or OGD condition. Scale bar = 20 µm. n = 3 per group. B). Representative flow cytometric histograms showing PLIN2 fluorescence intensity curves under different treatment conditions. Blank group cells received medium as no-treatment control. C). Percentage of PLIN2 + cells in BV2 cells under different treatment conditions. D). PLIN2 mean fluorescence intensity (MFI) in BV2 cells under different treatment conditions. E). Representative flow cytometric histograms showing Dextran 40 fluorescence intensity curves under different conditions. F). Percentage of Dextran 40 + cells in BV2 cells under different treatment conditions. G). Dextran 40 MFI under different treatment conditions. For flow cytometry, n = 6 per group; data are presented as mean ± SD; two-way ANOVA (OGD × drug) with Tukey’s multiple comparisons test; *p < 0.05, **p < 0.01, ***p < 0.001 vs. OGD and DMSO group; ### p < 0.001 vs. OGD + Blank group.

Article Snippet: DGAT1 inhibitor T863 (Cat# HY-32219, MedChemiExpress LCC, Monmouth Junction, NJ), and DGAT2 inhibitor PF-06424439 (Cat# HY-108341A, MCE) were dissolved in DMSO and used at 30 μM and 40 μM, respectively.

Techniques: Expressing, Control, Fluorescence, Flow Cytometry

A). Representative images of BODIPY (green) and IL-1β (white) expression in BV2 cells following DGAT inhibitor treatment. BV2 cells were treated with DGAT1 inhibitor T863 or DGAT2 inhibitor PF-06424439 (PF) or DMSO vehicle control under normoxic control or OGD condition. Scale bar = 20 µm. n = 3 per group. B). Representative flow cytometric histograms showing BODIPY fluorescence intensity curves in BV2 cells under different treatment conditions. Blank group cells received medium as no-treatment control. C). Percentage of BODIPY + cells in BV2 cells under different treatment conditions. D). BODIPY mean fluorescence intensity (MFI) under different treatment conditions. E). Representative flow cytometric histograms showing IL-1β fluorescence intensity curves under different treatment conditions. F). Percentage of IL-1β + cells in BV2 cells under different treatment conditions. G). IL-1β MFI in BV2 cells under different treatment conditions. For flow cytometry, n = 6 per group; data are presented as mean ± SD; two-way ANOVA (OGD × drug) with Tukey’s multiple comparisons test; *p < 0.05, **p < 0.01, ***p < 0.001 vs. OGD and DMSO group; ### p < 0.001 vs. OGD + Blank.

Journal: bioRxiv

Article Title: Accumulation of Lipid Droplets in Microglia following Neonatal Brain Hypoxia-Ischemia

doi: 10.64898/2026.07.18.739219

Figure Lengend Snippet: A). Representative images of BODIPY (green) and IL-1β (white) expression in BV2 cells following DGAT inhibitor treatment. BV2 cells were treated with DGAT1 inhibitor T863 or DGAT2 inhibitor PF-06424439 (PF) or DMSO vehicle control under normoxic control or OGD condition. Scale bar = 20 µm. n = 3 per group. B). Representative flow cytometric histograms showing BODIPY fluorescence intensity curves in BV2 cells under different treatment conditions. Blank group cells received medium as no-treatment control. C). Percentage of BODIPY + cells in BV2 cells under different treatment conditions. D). BODIPY mean fluorescence intensity (MFI) under different treatment conditions. E). Representative flow cytometric histograms showing IL-1β fluorescence intensity curves under different treatment conditions. F). Percentage of IL-1β + cells in BV2 cells under different treatment conditions. G). IL-1β MFI in BV2 cells under different treatment conditions. For flow cytometry, n = 6 per group; data are presented as mean ± SD; two-way ANOVA (OGD × drug) with Tukey’s multiple comparisons test; *p < 0.05, **p < 0.01, ***p < 0.001 vs. OGD and DMSO group; ### p < 0.001 vs. OGD + Blank.

Article Snippet: DGAT1 inhibitor T863 (Cat# HY-32219, MedChemiExpress LCC, Monmouth Junction, NJ), and DGAT2 inhibitor PF-06424439 (Cat# HY-108341A, MCE) were dissolved in DMSO and used at 30 μM and 40 μM, respectively.

Techniques: Expressing, Control, Fluorescence, Flow Cytometry

The apoptosis rate of HT22 cells following treatment with lipid synthesis inhibitors and lipid droplet inhibitors using flow cytometry. (A, B) Apoptosis in HT22 cells (A) and MA (B) were assessed after 24 hours of treatment with Lipofectamine 2000 (2 µL), siPLIN5 (30 nM), T863 (20 µM), and firsocostat (10 µM) ( n = 3 independent experiments). (C) Apoptosis was assessed by Annexin V-FITC/PI staining. HT22 cells were then subjected to OA treatment for 24 hours. Flow cytometry was used to measure cell apoptosis rates at varying OA concentrations ( n = 3 independent experiments). (D, E) Apoptosis rates in monocultured (D) and cocultured (E) HT22 cells were measured after 24 hours of treatment ( n = 3 independent experiments). (F, G) Apoptosis rates in monocultured (F) and cocultured (G) MA were measured after 24 hours of treatment ( n = 3 independent experiments). (H) After 24 hours of siRNA treatment, MA in each group were treated for an additional 24 hours according to their specific grouping. The total apoptosis rate of the cells was then measured ( n = 3 independent experiments). (I) Western blot analysis was conducted to assess the expression levels of PLIN5, caspase-1, and caspase-1 p20 in MA. (J) Quantitative analysis of apoptosis rates in cocultured astrocytes ( n = 3 independent experiments) (corresponding to H). (K, L) Quantitative analysis of PLIN5 (K) and caspase-1 p20 (L). Relative protein expression was normalized to β-actin ( n = 3 independent experiments) (corresponding to I). (M) Quantitative analysis of LDs ( n = 3 independent experiments) (corresponding to N). (N) After 24 hours of treatment, immunofluorescence was used to detect LDs in cocultured astrocytes. Scale bar: 20 µm (40× magnification). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 (one-way analysis of variance followed by Tukey’s post hoc test [A–G and J–M]). DAPI: 4′,6-Diamidino-2-phenylindole; LDs: lipid droplets; MA: mouse astrocyte; ns: not significant; OA: oleic acid; PI: propidium iodide.

Journal: Neural Regeneration Research

Article Title: Lactate alleviates early brain damage after subarachnoid hemorrhage: Regulation of lipid metabolism

doi: 10.4103/NRR.NRR-D-24-01543

Figure Lengend Snippet: The apoptosis rate of HT22 cells following treatment with lipid synthesis inhibitors and lipid droplet inhibitors using flow cytometry. (A, B) Apoptosis in HT22 cells (A) and MA (B) were assessed after 24 hours of treatment with Lipofectamine 2000 (2 µL), siPLIN5 (30 nM), T863 (20 µM), and firsocostat (10 µM) ( n = 3 independent experiments). (C) Apoptosis was assessed by Annexin V-FITC/PI staining. HT22 cells were then subjected to OA treatment for 24 hours. Flow cytometry was used to measure cell apoptosis rates at varying OA concentrations ( n = 3 independent experiments). (D, E) Apoptosis rates in monocultured (D) and cocultured (E) HT22 cells were measured after 24 hours of treatment ( n = 3 independent experiments). (F, G) Apoptosis rates in monocultured (F) and cocultured (G) MA were measured after 24 hours of treatment ( n = 3 independent experiments). (H) After 24 hours of siRNA treatment, MA in each group were treated for an additional 24 hours according to their specific grouping. The total apoptosis rate of the cells was then measured ( n = 3 independent experiments). (I) Western blot analysis was conducted to assess the expression levels of PLIN5, caspase-1, and caspase-1 p20 in MA. (J) Quantitative analysis of apoptosis rates in cocultured astrocytes ( n = 3 independent experiments) (corresponding to H). (K, L) Quantitative analysis of PLIN5 (K) and caspase-1 p20 (L). Relative protein expression was normalized to β-actin ( n = 3 independent experiments) (corresponding to I). (M) Quantitative analysis of LDs ( n = 3 independent experiments) (corresponding to N). (N) After 24 hours of treatment, immunofluorescence was used to detect LDs in cocultured astrocytes. Scale bar: 20 µm (40× magnification). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 (one-way analysis of variance followed by Tukey’s post hoc test [A–G and J–M]). DAPI: 4′,6-Diamidino-2-phenylindole; LDs: lipid droplets; MA: mouse astrocyte; ns: not significant; OA: oleic acid; PI: propidium iodide.

Article Snippet: T863 (MCE, Cat# HY-32219) was used to target triglyceride synthesis.

Techniques: Flow Cytometry, Staining, Western Blot, Expressing, Immunofluorescence