Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
Eur J Pharmacol. 2019 Sep 5;858:172469. doi: 10.1016/j.ejphar.2019.172469. Epub 2019 Jun 22.
The role of hepatic free cholesterol (FC) in nonalcoholic steatohepatitis (NASH) is raised up and the intervention with cholesterol synthesis will be a potential therapeutic target. This study investigated the hepatoprotective effect of mevalonic acid pathway inhibition by Zoledronic acid (ZA) on the hepatic changes associated with high fat diet (HFD) in rats.Thirty two male Wistar rats were used. They were divided into 2 groups: (I) control naïve (II) NASH: induced by HFD for 12 weeks, this group is subdivided into (A) NASH untreated (B)NASH + ZA (50ug/kg/week) i.p. for 12 weeks (C) NASH + ZA (100μg/kg/week) i.p. for 12 weeks. Portal pressure (PP), liver enzymes AST and ALT, serum glucose, lipid profile, hepatic levels of tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), FC and triglyceride (TG), histopathological changes and expression of both hepatic alpha smooth muscle actin (α-SMA) and Caspase-3 were measured. ZA significantly prevented portal hypertension, worsening in liver function, and dyslipidemia. The hepatic levels of TNF-α, VEGF, FC and TG were significantly decreased in comparison to NASH untreated group. ZA hindered the histopathological changes induced by HFD. ZA inhibited the expression of hepatic α-SMA and Caspase-3 with significant difference favor the high dose intervention. ZA in a dose related manner prevents the hepatic pathological effects of chronic HFD ingestion in rats. This may be largely mediated by its ability to reduce TNF-α and hepatic FC.
非酒精性脂肪性肝炎(NASH)中肝游离胆固醇(FC)的作用备受关注,抑制胆固醇合成将成为一种有潜力的治疗靶点。本研究旨在探讨唑来膦酸(ZA)抑制甲羟戊酸途径对高脂肪饮食(HFD)诱导的大鼠肝脏变化的保护作用。
使用 32 只雄性 Wistar 大鼠。将其分为 2 组:(I)对照组(II)NASH:用 HFD 诱导 12 周,该组进一步分为(A)NASH 未治疗组(B)NASH+ZA(50μg/kg/周)腹腔注射 12 周(C)NASH+ZA(100μg/kg/周)腹腔注射 12 周。测量门静脉压力(PP)、肝酶 AST 和 ALT、血清葡萄糖、血脂谱、肝组织肿瘤坏死因子-α(TNF-α)、血管内皮生长因子(VEGF)、FC 和三酰甘油(TG)水平、组织病理学变化以及肝α平滑肌肌动蛋白(α-SMA)和 Caspase-3 的表达。ZA 显著预防了门脉高压、肝功能恶化和血脂异常。与 NASH 未治疗组相比,ZA 显著降低了 TNF-α、VEGF、FC 和 TG 的肝组织水平。ZA 阻碍了 HFD 诱导的组织病理学变化。ZA 抑制了肝α-SMA 和 Caspase-3 的表达,高剂量干预具有显著差异。ZA 以剂量相关的方式预防了大鼠慢性 HFD 摄入引起的肝病理效应。这可能主要是通过其降低 TNF-α和肝 FC 的能力介导的。