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首页> 外文期刊>RSC Advances >Catalpol prevents alteration of cholesterol homeostasis in non-alcoholic fatty liver disease via?attenuating endoplasmic reticulum stress and NOX4 over-expression
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Catalpol prevents alteration of cholesterol homeostasis in non-alcoholic fatty liver disease via?attenuating endoplasmic reticulum stress and NOX4 over-expression

机译：Catalpol通过减轻内质网应激和NOX4过表达来预防非酒精性脂肪肝疾病中胆固醇稳态的改变

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Catalpol is a natural product isolated from the root of Rehmannia glutinosa, and contributes to multiple pharmacological functions. Here, we showed the protective effects of catalpol against the alteration of cholesterol homeostasis in non-alcoholic fatty liver disease (NAFLD), and further investigated the role of endoplasmic reticulum stress (ER stress) and NOX4-mediated inhibition in alteration of cholesterol homeostasis by catalpol in NAFLD. NAFLD was induced in vivo in C57BL/6J mice by feeding with high-fat diet (HFD) for 12 weeks or in vitro in HepG2 cells by stimulating with palmitate (PA) for 24 hours. The results showed that catalpol reduced hepatic lipid accumulation, ER stress, NOX4-mediated oxidative stress and alteration of cholesterol homeostasis in HFD-induced C57BL/6J mice and PA-induced HepG2 cells. In addition, NOX4 over-expression was reduced by ER stress inhibitor TUDCA and GRP78 over-expression was down-regulated by NOX4 inhibitor DPI in PA-induced HepG2 cells. The results demonstrated that ER stress and NOX4 over-expression regulated each other in PA-induced NAFLD. Furthermore, administrating with ER stress inhibitor or NOX4 inhibitor attenuated lipid accumulation and alteration of cholesterol homeostasis in NAFLD induced by PA. Therefore, catalpol conferred prevention against alteration of cholesterol homeostasis in NAFLD at least partly through attenuating both ER stress and NOX4 over-expression.
机译：Catalpol是从 Rehmannia glutinosa 的根中分离出来的天然产物，并具有多种药理功能。在这里，我们展示了梓醇对非酒精性脂肪肝疾病（NAFLD）中胆固醇稳态变化的保护作用，并进一步研究了内质网应激（ER应激）和NOX4介导的抑制作用在胆固醇代谢中的作用。 NAFLD中的catalpol。通过饲喂高脂饮食（HFD）12周或通过用棕榈酸酯（PA）刺激HepG2细胞体外体外诱导C57BL / 6J小鼠体内体内 24小时。结果表明，梓醇可以降低HFD诱导的C57BL / 6J小鼠和PA诱导的HepG2细胞的肝脂质蓄积，内质网应激，NOX4介导的氧化应激和胆固醇稳态的改变。另外，在ER诱导的HepG2细胞中，ER应激抑制剂TUDCA减少了NOX4的过表达，而NOX4抑制剂DPI下调了GRP78的过表达。结果表明，在PA诱导的NAFLD中，ER应激和NOX4的过量表达相互调节。此外，与ER应激抑制剂或NOX4抑制剂一起给药可减轻PA诱导的NAFLD中脂质蓄积和胆固醇稳态的改变。因此，catalpol至少部分地通过减弱ER应激和NOX4过表达来预防NAFLD中胆固醇稳态的改变。

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