We studied the effects of alfalfa saponin extract（ASE） on low density lipoprotein receptor（Ldlr）, liver X receptor α（LXRα）, and farnesoid X receptor（FXR） in normal and hyperlipidemic Buffalo rat liver（BRL）...We studied the effects of alfalfa saponin extract（ASE） on low density lipoprotein receptor（Ldlr）, liver X receptor α（LXRα）, and farnesoid X receptor（FXR） in normal and hyperlipidemic Buffalo rat liver（BRL） cells. Normal and hyperlipidemic BRL cells were divided into eight groups： normal, or normal cells treated with 50, 100, and 150 mg/L ASE, hyperlipidemic, or hyperlipidemic cells treated with 50, 100, and 150 mg/L ASE. After treatment for 24 h, Ldlr, LXRα, and FXR m RNA expression levels were measured by quantitative real-time polymerase chain reaction（q RT-PCR）. Data showed that m RNA expression of Ldlr in normal BRL cells was significantly up-regulated by ASE treatment and m RNA expressions of LXRα and FXR were significantly down-regulated both in normal and hyperlipidemic BRL cells after ASE treatment. Thus, ASE might ameliorate hepatic steatosis by regulating genes involved in cholesterol metabolism, including up-regulation of Ldlr as well as down-regulation of LXRα and FXR.展开更多
基金Project supported by the National Natural Science Foundation of China(No.31301983)the Earmarked Fund for Modern Agro-industry Technology Research System of China(No.CARS-35)
文摘We studied the effects of alfalfa saponin extract（ASE） on low density lipoprotein receptor（Ldlr）, liver X receptor α（LXRα）, and farnesoid X receptor（FXR） in normal and hyperlipidemic Buffalo rat liver（BRL） cells. Normal and hyperlipidemic BRL cells were divided into eight groups： normal, or normal cells treated with 50, 100, and 150 mg/L ASE, hyperlipidemic, or hyperlipidemic cells treated with 50, 100, and 150 mg/L ASE. After treatment for 24 h, Ldlr, LXRα, and FXR m RNA expression levels were measured by quantitative real-time polymerase chain reaction（q RT-PCR）. Data showed that m RNA expression of Ldlr in normal BRL cells was significantly up-regulated by ASE treatment and m RNA expressions of LXRα and FXR were significantly down-regulated both in normal and hyperlipidemic BRL cells after ASE treatment. Thus, ASE might ameliorate hepatic steatosis by regulating genes involved in cholesterol metabolism, including up-regulation of Ldlr as well as down-regulation of LXRα and FXR.
