理气化痰祛瘀法抗非酒精性脂肪性肝炎大鼠的脂质过氧化损伤

目的]观察理气化痰祛瘀中药对非酒精性脂肪性肝炎（NASH）大鼠脂质过氧化反应的影响，探讨其防治NASH的作用机制。方法]高脂饮食喂养12周诱导Wistar大鼠建立NASH模型，以不同剂量的理气化痰祛瘀中药预防及治疗，检测大鼠血清及肝组织丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSHPX）的水平，光镜观察肝组织切片病理学改变。结果]模型大鼠肝组织出现了严重脂肪变和不同程度炎症细胞浸润。模型大鼠血及肝组织中MDA水平较正常大鼠显著升高，而SOD、GSH-PX活性则较正常大鼠显著降低。应用理气化痰祛瘀中药进行预防和治疗后，大鼠肝组织脂肪变程度和炎症活动程度较模型大鼠显著降低，同时血及肝组织MDA水平显著降低，而SOD、GSH-PX活性则显著提高。结论]理气化痰祛瘀法中药对NASH有防治作用，其作用机制可能与抑制脂质过氧化反应有关。

Effect of regulating qi to dissipate blood stasis and phlegm on relieving lipid peroxidation injury in rats with nonalcoholic steatohepatitis and its mechanism

Objective] To observe the effects of Chinese herbs of regulating qi to dissipate blood stasis and phlegm on lipid peroxidation reaction in rats with nonalcoholic steatohepatitis(NASH),and inquire into its mechanism of preventing and treating NASH.Methods] The model of NASH in Wistar rats was induced by a term of 12-week high fat diet,then prevented and treated by different doses of Chinese herbs of regulating qi to dissipate blood stasis and phlegm for 8 weeks.The amount of MDA,SOD,GSH-PX in serum and liver tissue was detected and the pathological changes in HE staining liver tissue were observed.Results] Compared with that of the normal group,the liver tissue appeared severely steatosis and gradually infiltrated with inflammation cells,and appeared necrosis in hepatocyte,percolate in portal area in the model group.The levels of MDA in serum and liver tissue of the model group obviously increased,while the active levels of SOD,GSH-PX obviously decreased.After prevented and treated by different doses of Chinese herbs of regulating qi to dissipate blood stasis and phlegm for 8 weeks,the steatosis and inflammation were obviously relieved,moreover,the levels of MDA in serum and liver tissue obviously decreased,while the active levels of SOD,GSH-PX obviously increased. Conclusion]Chinese herbs of regulating qi to dissipate blood stasis and phlegm can prevent and treat NASH to a certain degree,and the mechanism of which perhaps relates to preventing lipid peroxidation reaction.