Larsucosterol (trimethylamine) (Synonyms: DUR-928 (trimethylamine)) |
| رقم الكتالوجGC65936 |
Larsucosterol (DUR-928) ثلاثي ميثيل أمين ، مستقلب الكوليسترول ، هو مضاد قوي لمستقبلات الكبد X (LXR). Larsucosterol trimethylamine كمنظم داخلي قوي يقلل من تكون الدهون. يثبط Larsucosterol trimethylamine التخليق الحيوي للكوليسترول عن طريق خفض مستويات mRNA وتثبيط تنشيط SREBP-1.
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Sample solution is provided at 25 µL, 10mM.
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Larsucosterol (DUR-928) trimethylamine, a cholesterol metabolite, is a potent liver X receptor (LXR) antagonist. Larsucosterol trimethylamine as a potent endogenous regulator decreases lipogenesis. Larsucosterol trimethylamine inhibits the cholesterol biosynthesis via decreasing mRNA levels and inhibiting the activation of SREBP-1[1][2][3].
Larsucosterol (DUR-928; 0-25 μM; 8 h; HepG2 cells) trimethylamine inhibits cholesterol biosynthesis by decreasing HMG-CoA reductase mRNA levels and decreases free [14C] cholesterol in a dose-dependent manner[1].
Larsucosterol (0-25 μM; 6 h; HepG2 cells) trimethylamine inhibits HMG-CoA reductase expression by inhibition of both SREBP1 activation and expression in hepatocytes[1].
Larsucosterol (0-50 μM; 48 h) trimethylamine increases cell proliferation and decreases apoptosis in macrophages[2].
Larsucosterol (0-25 μM; 48 h; macrophages) trimethylamine inhibits activation of liver oxysterol receptor LXRα[2].
Cell Proliferation Assay[2]
| Cell Line: | Macrophages |
| Concentration: | 0, 5, 10, 15, 20, and 25 μM |
| Incubation Time: | 48 hours |
| Result: | Induces cell proliferation and relative cell number after treatment for 48 h were 120% at 25 μM. |
Apoptosis Analysis[2]
| Cell Line: | Macrophages |
| Concentration: | 0, 10, 20, 30, 40 and 50 μM |
| Incubation Time: | 48 hours |
| Result: | Did not significantly affect the numbers of apoptotic or live cells. |
Western Blot Analysis[1]
| Cell Line: | HepG2 cells |
| Concentration: | 0, 3, 6, 12, and 25 μM |
| Incubation Time: | 6 hours |
| Result: | Inhibited the activation of SREBP-1 and SREBP-2, and subsequently inhibit the expression HMG-CoA reductase. |
Western Blot Analysis[2]
| Cell Line: | Macrophages |
| Concentration: | 0, 3, 6, 12, and 25 μM |
| Incubation Time: | 48 hours |
| Result: | Decreased LXRα levels in the nuclei in a does-dependent manner. |
Larsucosterol (DUR-928; 25 mg/kg; i.p.; twice in 14 hours; C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model) trimethylamine reduces serum lipid levels in mice fed a high-fat diet[3].
Larsucosterol (25 mg/kg; i.p.; twice in 14 hours; C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model) trimethylamine suppressed the expression of the genes and inhibits ABCA1 expressionde. Larsucosterolcreases nuclear SREBP-1 Protein levels and cytoplasmic FAS and ACC1 protein levels in liver tissue[3].
Larsucosterol (25 mg/kg; i.p.; once every 3 days for 6 weeks; C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model) trimethylamine protects the liver from injury by suppressing hepatic inflammation[3].
| Animal Model: | Female C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model[3] |
| Dosage: | 25 mg/kg |
| Administration: | Intraperitoneal injection; twice in 14 hours |
| Result: | Decreased plasma TG, CHOL, and HDL-C by 40, 15, and 20%, respectively. Reduced the mRNA levels of SREBP-1c, ACC1, and FAS by 46, 57, and 49%, respectively. Suppressed ABCA1 expression. Suppressed nuclear SREBP-1, cytoplasmic ACC1, and FAS protein levels by 74, 58, and 47%, respectively. |
| Animal Model: | Female C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model[3] |
| Dosage: | 25 mg/kg |
| Administration: | Intraperitoneal injection; once every 3 days for 6 weeks |
| Result: | Decreased plasma cholesterol levels. Reduced serum alkaline phosphatase, ALT, and AST levels. |
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