解毒化瘀Ⅱ方对暴发性肝衰竭大鼠肝线粒体的保护作用  

Protective Effect of the Detoxification and Dissipation Blood Stasis Formula Ⅱ on Hepatic Mitochondria in Rats with Fulminant Hepatic Failure

作　　者：毛德文[1] 邱华[1] 马银瑶[1] 农朝赞[1] 余晶[1] 

机构地区：[1]广西中医学院第一附属医院中医肝病治疗中心,广西南宁530023

出　　处：《中华中医药学刊》2007年第5期907-909,共3页Chinese Archives of Traditional Chinese Medicine

基　　金：国家自然科学基金项目(30360125);广西自然科学基金项目(桂科自0542103)

摘　　要：目的:研究解毒化瘀Ⅱ方对暴发性肝衰竭大鼠肝线粒体的保护作用,并从抗脂质过氧化探讨其作用机制。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,SPF级Wistar大鼠84只,随机分为空白组,模型组,解毒化瘀Ⅱ方低、中、高剂量组,安宫牛黄丸组,乳果糖组。造模前3天开始灌胃给药,2次/天,间隔12h,共给药5天12h;测定各组大鼠肝线粒的肿胀度、肝脏坏死面积及肝线粒体内MDA、SOD、GSH、NO。结果:模型组肝线粒体对外源性钙离子引发肿胀的敏感性下降、肝细胞大量坏死,肝线粒体内MDA含量急剧升高,SOD活性及GSH、NO含量显著下降,与空白组比较差异有统计学意义(P<0.01);解毒化瘀Ⅱ方各组能提高肝线粒体对外源性钙离子引发肿胀的敏感性、减少肝脏坏死面积,抑制肝线粒体内脂质过氧化物MDA的生成,恢复SOD的活力及GSH、NO含量,并呈现量效关系。结论:在暴发性肝衰竭致病过程中,肝线粒体内的NO主要起保护性作用;解毒化瘀Ⅱ方对暴发性肝衰竭肝线粒体具有较强的保护作用,可能是通过拮抗脂质过氧化来实现。Objective： To research Protective effect of the Detoxification and Dissipation Blood Stasis Formula Ⅱ on hepatic mitochondria in Rats with fulminant hepatic failure, and to explore its mechanism from anti - lipid peroxidation. Methods： The fulminant hepatic failure rat models were induced by injection thioacetamide （TAA）. Eighty four SPF Wistar rats were divided into seven groups by random： blank group, modle group, low dose group, middle dose group, high dose group, the lactulose treating group, and the ＂ Bezoare pill for resurrection＂ treating group. Administration of gastric infusion was executed 3 days before model -making, twice a day with an interval of 12 hours, 5 days 12 hours in total. We tested hepatic mitochondria swelling, liver necrosis area and hepatic mitochondrial MDA, SOD, GSH, NO. Results： we notice that in model group the sensitivity of swelling to the exotic Ca^2＋ in hepatic mitochondria reduced,large bulk of hepatocyte necrosed , the content of hepatic mitochondrial MDA increased rapidly, however the activity of SOD and the content of GSH, NO decreased rapidly. Compared with blank group, there is statistical significance（ P 〈 0. 01 ）. Twelve hours after intragastric administration the detoxification and dissipation blood stasis formula Ⅱ, the medicine was able to increase the sensitivity of swelling to the exotic Ca^2 ＋ , decrease liver necrosis area and restrain produce of hepatic mitochondrial lipid peroxidatide MDA, retrieve the activity of SOD, increase the content of GSH, NO and reduce liver necrosis area. Moreover it shows dose - effect relation. Conclusions ： The role of NO is protector in hepatic mitochondrial . The detoxification and dissipation blood stasis formula Ⅱ protected hepatic mitochondrial in Fulminant hepatic failure rats. This medical action may be due to it resist hepatic mitochondrial lipid peroxidation.

关 键 词：暴发性肝衰竭 脂质过氧化 一氧化氮 肝线粒体 解毒化瘀Ⅱ方 

分 类 号：R285[医药卫生—中药学] R575.3[医药卫生—中医学]