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目的:研究绞股蓝多糖对四氯化碳诱导大鼠肝损伤的保护作用。方法:大鼠以50%CCl4花生油溶液按1 mL·kg-1ig,连续4周建立实验性肝损伤模型。随机分为4组:模型对照组、联苯双酯组、绞股蓝多糖低、高剂量组,并设正常对照组。ig绞股蓝多糖40,80 g·kg-1,联苯双酯40 mg·kg-1,正常对照组及模型组ig给予等量生理盐水,连续ig 30 d。末次给药24 h后取材,检测大鼠血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)的含量,逆转录聚合酶链式反应(RT-PCR)法测定肝组织中诱导型一氧化氮合酶(iNOS)mRNA的表达,Western blot法测定肝组织中B细胞淋巴瘤/白血病-2基因(Bcl-2)/Bcl-2相关X蛋白(Bax)凋亡相关蛋白的表达,并观察肝组织病理学变化。结果:与模型组比较,绞股蓝多糖低、高剂量给药组有效降低肝损伤大鼠血清中AST(85.28±4.09,72.49±3.62)U.L-1,ALT(75.31±3.95),(58.26±4.83)U.L-1水平(P<0.05),下调组织中iNOS mRNA的表达(P<0.05)。治疗后大鼠肝组织中Bcl-2/Bax蛋白水平均有所升高(P<0.05),并减轻肝损伤病情。结论:绞股蓝多糖对CCl4诱导的大鼠肝损伤具有一定保护作用,其机制可能与其抑制细胞毒作用以及抗凋亡途径有关。
Objective: To study the protective effect of Gynostemma Pentaphyllum polysaccharide against carbon tetrachloride-induced liver injury in rats. Methods: Rats were treated with 50% CCl4 peanut oil solution at 1 mL · kg-1ig for 4 weeks to establish experimental liver injury model. Randomly divided into 4 groups: model control group, bifendate group, Gynostemma polysaccharide low and high dose group, and set the normal control group. ig Gynostemma polysaccharides 40,80 g · kg-1, bifendate 40 mg · kg-1, the normal control group and model group ig given the same amount of saline for ig 30 d. Serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured 24 h after the last administration, and induced in liver tissue by reverse transcriptase-polymerase chain reaction (RT-PCR) The expression of iNOS mRNA was detected by Western blot. The expressions of Bcl-2 / Bcl-2 protein in liver tissues were detected by Western blot , And observed the pathological changes of liver tissue. Results: Compared with model group, low and high doses of Gypenosides could effectively reduce the serum levels of AST (85.28 ± 4.09,72.49 ± 3.62), ALT (75.31 ± 3.95) and (58.26 ± 4.83) UL-1 level (P <0.05), and down-regulated the expression of iNOS mRNA (P <0.05). After treatment, Bcl-2 / Bax protein levels in rat liver tissue were increased (P <0.05), and liver damage was alleviated. CONCLUSION: Gynostemma polysaccharides can protect CCl4-induced liver injury in rats. The mechanism may be related to its inhibition of cytotoxicity and anti-apoptotic pathways.