Larsucosterol (DUR-928) 是一种胆固醇代谢物，是一种有效的肝 X 受体 (LXR) 拮抗剂。Larsucosterol 是一种有效的内源性脂肪生成调节剂。Larsucosterol 通过降低 mRNA 水平和抑制 SREBP-1 的激活抑制胆固醇的生物合成。
| 生物活性 | Larsucosterol (DUR-928), acholesterolmetabolite, is a potentliver X receptor (LXR)antagonist. Larsucosterol as a potent endogenous regulator decreases lipogenesis. Larsucosterol inhibits thecholesterolbiosynthesis via decreasing mRNA levels and inhibiting the activation of SREBP-1[1][2][3]. |
体外研究
(In Vitro) | Larsucosterol (DUR-928; 0-25 μM; 8 h; HepG2 cells) 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) inhibits HMG-CoA reductase expression by inhibition of both SREBP1 activation and expression in hepatocytes[1].
Larsucosterol (0-50 μM; 48 h) increases cell proliferation and decreases apoptosis in macrophages[2].
Larsucosterol (0-25 μM; 48 h; macrophages) 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, 5, 10, 15, 20, and 25 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. |
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体内研究
(In Vivo) | Larsucosterol (DUR-928; 25 mg/kg; i.p.; twice in 14 hours; C57BL/6J mice with nonalcoholic fatty liver diseases (NAFLD) model) 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) 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) 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; once every 3 days for 6 weeks | | Result: | Decreased plasma cholesterol levels.
Reduced serum alkaline phosphatase, ALT, and AST levels.
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| 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.
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| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | Please store the product under the recommended conditions in the Certificate of Analysis. |
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