Pharmacology and Toxicology Department, Faculty of Pharmacy, Tanta University, Tanta 31111, Egypt.
PPAR Res. 2013;2013:781348. doi: 10.1155/2013/781348. Epub 2013 Aug 12.
Background. Activation of PPAR α modulates cholesterol metabolism and suppresses bile acid synthesis. This study aims to evaluate the effect of PPAR α agonists, fenofibrate, bezafibrate, and gemfibrozil, on acute cholestasis induced by ethinylestradiol (EE) plus chlorpromazine (CPZ) in rats. Method. 100 male albino rats (150-200 gm) were divided randomly into 10 equal groups. Control group received 1% methylcellulose vehicle; disease group received CPZ plus EE for 5 consecutive days; four groups received either ursodeoxycholic acid, fenofibrate, bezafibrate, or gemfibrozil for 7 days; 2 days before EE + CPZ, three other groups received one of the three fibrates after GW6471, a selective PPAR α antagonist in addition to EE + CPZ. The final group received GW6471 alone. Results. The three fibrates showed marked reduction (P < 0.05) in serum levels of ALP, GGT, ALT, AST, total bile acids, bilirubin, TNF α , and IL-1 β and in hepatic malondialdehyde level as well as a significant increase in bile flow rate (P < 0.05) in addition to improvements in histopathological parameters compared to diseased group. In groups which received GW6471, these effects were completely abolished with fenofibrate and partially blocked with bezafibrate and gemfibrozil. Conclusion. Short-term administration of fibrates to EE/CPZ-induced intrahepatic cholestatic rats exerted beneficial effects on hepatocellular damage and apoptosis. Fenofibrate anticholestatic effect was solely PPAR α dependent while other mechanisms played part in bezafibrate and gemfibrozil actions.
背景。激活过氧化物酶体增殖物激活受体 α(PPAR α)可调节胆固醇代谢并抑制胆汁酸合成。本研究旨在评估 PPAR α 激动剂非诺贝特、苯扎贝特和吉非罗齐对雌二醇(EE)加氯丙嗪(CPZ)诱导的大鼠急性胆汁淤积的影响。方法。将 100 只雄性白化大鼠(150-200 克)随机分为 10 组。对照组给予 1%甲基纤维素载体;疾病组连续 5 天给予 CPZ 加 EE;四组分别给予熊去氧胆酸、非诺贝特、苯扎贝特或吉非罗齐 7 天;在给予 EE+CPZ 前 2 天,另外三组在给予 EE+CPZ 后给予三种纤维酸之一 GW6471,一种选择性 PPAR α 拮抗剂。最后一组单独给予 GW6471。结果。三种纤维酸均显著降低(P<0.05)血清碱性磷酸酶(ALP)、γ-谷氨酰转移酶(GGT)、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、总胆汁酸、胆红素、肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)水平,以及肝丙二醛水平,并显著增加胆汁流速(P<0.05),与疾病组相比,组织病理学参数也有所改善。在给予 GW6471 的组中,这些作用完全被非诺贝特消除,部分被苯扎贝特和吉非罗齐阻断。结论。短期给予纤维酸酯类药物可改善 EE/CPZ 诱导的大鼠肝内胆汁淤积性肝损伤和细胞凋亡。非诺贝特的抗胆汁淤积作用仅依赖于 PPAR α,而其他机制在苯扎贝特和吉非罗齐的作用中发挥了作用。