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Protective effects of ginseng total saponins against hepatic ischemia/reperfusion injury in experimental obstructive jaundice rats

机译:人参总皂苷对实验性梗阻性黄疸大鼠肝缺血/再灌注损伤的保护作用

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Context: Ginseng, the root of Panax ginseng C.A. Meyer (Araliaceae), is one of the most extensively used herbs for stroke and chronic debilitating conditions in East Asian countries. Ginsenosides (GS) are the main bioactive compounds for ginseng's efficacy, but the mechanisms have not been fully clarified. Objective: To investigate hepatoprotective effects of GS against ischemia/reperfusion (IR) injury in the experimental obstructive jaundice rats. Materials and methods: GS was fed to cholestatic rats with IR injury daily for 6?d at a dose of 1.10?g/kg. Levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by colorimetric method. Apoptosis was measured quantitatively by the terminal transferase UTP nick end-labeling method. Protein expression of Bax and Bcl-2 was detected by immunohistochemistry. Results and discussion: After intervention of GS to cholestatic rats with IR injury, the levels of activating blood flow were significantly improved, and the levels of serum ALT were decreased 1.7-times, AST decreased 1.3-times, but SOD activities were increased 1.1-times compared with those of the model rats. It could also reverse histopathological changes and inhibit IR-induced apoptosis of hepatic tissues via decrease of Bax/Bcl-2 ratio (from 2.87?±?0.57 to 1.65?±?0.29). Oral administration of GS in a dosage of 26.4?g/kg did not lead to toxic effects in rats. Conclusion: GS attenuated the IR injury in the presence of cholestasis and could be considered for the clinical treatment of cholestasis.
机译:背景:人参,人参C.A.的根梅耶(菊科)是东亚国家中风和慢性衰弱性疾病中使用最广泛的草药之一。人参皂苷(GS)是提高人参功效的主要生物活性化合物,但其机理尚未完全阐明。目的:探讨GS对实验性梗阻性黄疸大鼠肝缺血/再灌注损伤的保护作用。材料和方法:每天以1.10μg/ kg的剂量将GS喂给患有IR损伤的胆汁淤积大鼠,持续6 d。用比色法测定丙氨酸氨基转移酶(ALT),天冬氨酸氨基转移酶(AST),超氧化物歧化酶(SOD)和丙二醛(MDA)的含量。通过末端转移酶UTP缺口末端标记法定量测定细胞凋亡。通过免疫组织化学检测Bax和Bcl-2的蛋白表达。结果与讨论:GS干预胆汁淤积性IR损伤大鼠后,活化血流水平明显改善,血清ALT下降1.7倍,AST下降1.3倍,SOD活性提高1.1-与模型大鼠比较。它还可以通过降低Bax / Bcl-2比值(从2.87?±?0.57降至1.65?±?0.29)来逆转组织病理学变化并抑制IR诱导的肝组织凋亡。口服GS 26.4?g / kg不会对大鼠产生毒性作用。结论:GS可减轻胆汁淤积时的IR损伤,可考虑用于胆汁淤积的临床治疗。

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