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目的:观察血清肿瘤坏死因子-α(TNF-α)在大鼠酒精性肝病(ALD)形成中的动态变化及中药三七对其的影响。方法:110只雄性SD大鼠随机分为正常组30只,模型组35只,三七高剂量组、三七低剂量组和硫普罗宁组各15只,连续14周白酒-玉米油-吡唑混合液灌胃建立ALD模型,造模同时三七高、低剂量组和硫普罗宁组分别灌服1.2g.kg-1.d-1、0.6g.kg-1.d-1的三七粉及0.1g.kg-1.d-1的硫普罗宁;4周末、8周末、14周末正常组分别随机处死大鼠10只,模型组分别随机处死大鼠8只用于肝脏病理变化的动态观察;14周末处死剩余所有大鼠,光镜观察肝组织脂肪变、炎症及纤维化程度,酶法测定血清ALT、AST水平,脂酶法测定血脂(TG、CHOL、HDL-C、LDL-C),ELISA法测定血清TNF-α水平。结果:与同期正常组相比,各时间点模型组大鼠肝组织脂肪变及炎症程度计分明显增高(P<0.01);14周末血清TNF-α水平明显增加(P<0.01);大鼠血清TNF-α水平与肝脂肪变及炎症程度均明显正相关(r分别为0.65、0.77,P<0.01);实验结束时模型组大鼠血清ALT、AST及CHOL、HDL-C水平较正常组明显增高(P<0.01)。三七高、低剂量组及硫普罗宁组大鼠肝组织脂肪变及炎症程度、血清ALT、AST水平和血清TNF-α水平较模型组明显减轻或降低(P<0.01或0.05),对血脂未见明显影响(P>0.05)。结论:用白酒-玉米油-吡唑混合液灌胃14周能成功复制大鼠ALD模型;血清TNF-α水平在大鼠ALD形成过程中逐步增加并主要与炎症程度相关;三七可明显减轻ALD大鼠肝组织脂肪变和炎症程度,降低血清TNF-α水平,后者可能是三七有效防治ALD的机制之一。
OBJECTIVE: To observe the dynamic changes of serum tumor necrosis factor-α (TNF-α) in rats with alcoholic liver disease (ALD) and the effects of Sanqi on them. METHODS: One hundred and ten male Sprague-Dawley rats were randomly divided into normal group (n = 30), model group (n = 35), sanqi high-dose group, sanqi low-dose group, and tiopronin group (n = 15) for 14 consecutive weeks of liquor-corn oil-pyrazole. The ALD model was established by intragastric administration of azole mixture. At the same time, the high-dose and low-dose groups of Sanqi and the tiopronin group were fed with 1.2g.kg-1.d-1 and 0.6g.kg-1.d-1 respectively. Seven powders and tiopronin 0.1g.kg-1.d-1; normal rats in the 4th, 8th, and 14th weekends were randomly killed and 10 rats in the model group were randomly executed for liver pathological changes. Dynamic observation; All rats were sacrificed at the end of the 14th week. The degree of liver steatosis, inflammation and fibrosis were observed by light microscopy. Serum ALT, AST levels were determined by enzymatic method, and lipids (TG, CHOL, HDL-C, LDL) were determined by lipase method. -C) ELISA for determination of serum TNF-α levels. RESULTS: Compared with the normal group at the same time, the scores of steatosis and inflammation in the hepatic tissue of the model group were significantly higher at each time point (P<0.01); the levels of serum TNF-α were significantly increased at the end of the 14th week (P<0.01); Serum TNF-α levels were positively correlated with liver steatosis and inflammation (r = 0.65, 0.77, P <0.01). At the end of the experiment, serum ALT, AST and CHOL, HDL-C levels in the model group were higher than those in the normal group. Significantly increased (P <0.01). The hepatic steatosis and inflammation, serum ALT, AST levels and serum TNF-α levels were significantly reduced or decreased (P<0.01 or 0.05) in the Panax notoginseng high- and low-dose group and tiopronin group compared to the model group. No significant effect (P>0.05). Conclusion: The rat model of ALD can be successfully established by intragastric administration of liquor-corn oil-pyrazole mixture for 14 weeks. Serum TNF-α level is gradually increased during the formation of ALD in rats and is mainly related to the degree of inflammation. Panax notoginseng can be significantly reduced. The degree of steatosis and inflammation in liver tissue of ALD rats decreased serum TNF-α levels, which may be one of the mechanisms of effective prevention and treatment of ALD by Panax notoginseng.