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目的研究解毒化淤Ⅱ方的中药配方颗粒对暴发性肝衰竭大鼠肝线粒体内脂质过氧化作用的影响。方法采用皮下注射硫代乙酰胺(TAA)法复制暴发性肝衰竭大鼠模型。取Wistar大鼠84只,随机分为空白组、模型组、解毒化淤Ⅱ方中药配方颗粒剂(低、中、高剂量组)、安宫牛黄丸组、乳果糖组,造模前3d开始灌胃给药,2次.d-1,间隔12h,共给药11次;造模完成12h后,测定各组大鼠肝线粒体内丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、还原型谷胱甘肽(GSH)、一氧化氮(NO)及肝脏的坏死面积。结果解毒化淤Ⅱ方中药配方颗粒剂能显著减少肝脏坏死面积,抑制肝线粒体内脂质过氧化终产物MDA的生成,恢复SOD、CAT的活力,提高GSH、NO的含量,并呈量效关系,与模型组比较差异有统计学意义(P<0.05或P<0.01);肝脏的坏死面积与肝线粒体内MDA呈正相关关系,与SOD、CAT、GSH、NO呈负相关关系。结论解毒化淤Ⅱ方中药配方颗粒剂对暴发性肝衰竭肝细胞具有较强的保护作用,其作用机制可能是通过拮抗脂质过氧化来实现。
Objective To study the effects of Jiedu Huayu II Formula on the lipid peroxidation of hepatic mitochondria in rats with fulminant hepatic failure. Methods Subcutaneous injection of thioacetamide (TAA) was used to replicate the rat model of fulminant hepatic failure. 84 Wistar rats were randomly divided into blank group, model group, detoxification and siltation II prescription granules (low, medium, and high dose group), Angong Niuhuangwan group, and lactulose group, starting 3 days before modeling. Intragastric administration, 2 times. D-1, interval 12h, co-administration 11 times; 12 hours after model establishment, determination of malondialdehyde (MDA), superoxide dismutase (SOD) in liver mitochondria of rats in each group. , catalase (CAT), reduced glutathione (GSH), nitric oxide (NO), and liver necrosis area. RESULTS Detoxification Huayu II Formula granules can significantly reduce the area of liver necrosis, inhibit the production of MDA in lipid oxidative end products in liver mitochondria, restore the activity of SOD and CAT, increase the content of GSH and NO, and show a dose-effect relationship. There was a statistically significant difference between the model group and the model group (P<0.05 or P<0.01). The liver necrosis area was positively correlated with mitochondrial MDA, and negatively correlated with SOD, CAT, GSH, and NO. Conclusion Detoxification and siltation II formula granules have a strong protective effect on hepatocytes of fulminant hepatic failure, and its mechanism may be achieved by antagonizing lipid peroxidation.