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目的观察低分子量肝素对长期摄入高脂饮食所致大鼠非酒精性脂肪性肝炎的干预作用,探讨其机制。方法雄性SD大鼠40只,随机分为正常对照组(n=10)及模型组(n=10),模型组喂以高脂饮食共8周;其余20只在高脂饮食8周后分为低分子肝素低剂量治疗组(n=10),在继续高脂饲料喂养的基础上,加用低分子量肝素治疗[50IU/(kg·d)];低分子肝素高剂量治疗组(n=10),在继续高脂饲料喂养基础上,加用低分子量肝素治疗[200IU/(kg·d)],共治疗2周。结果低分子肝素高剂量组[200IU/(kg·d)]在抑制肝脏慢性炎症、防止肝脏脂质堆积方面较模型组有统计学差异,而低剂量组[50IU/(kg·d)]作用不如高剂量组作用明显。结论低分子量肝素能够抑制肝脏慢性炎症的发生,调节脂质在肝脏中的堆积,有治疗非酒精性脂肪性肝炎的作用,且其作用效果与剂量相关。其作用机制可能是调节血脂,降低血清中TNF-α的水平。
Objective To observe the intervention effect of low molecular weight heparin on nonalcoholic steatohepatitis induced by long-term high-fat diet in rats and to explore its mechanism. Methods Forty male Sprague-Dawley rats were randomly divided into normal control group (n = 10) and model group (n = 10). The model group was fed a high-fat diet for 8 weeks. The remaining 20 rabbits were fed with high fat diet for 8 weeks Low-molecular-weight heparin low-dose treatment group (n = 10), low-molecular-weight heparin treatment [50IU / (kg · d) 10). On the basis of continuing high fat diet, low molecular weight heparin (200 IU / (kg · d)] was added for 2 weeks. Results The high-dose low-molecular-weight heparin group [200 IU / (kg · d)] had a statistically significant effect on suppressing chronic liver inflammation and preventing hepatic lipid accumulation compared with the model group [50 IU / (kg · d)] Not as high-dose group obvious effect. Conclusion Low molecular weight heparin can inhibit the occurrence of chronic inflammation in the liver, regulate the accumulation of lipids in the liver, and treat non-alcoholic steatohepatitis, and its effect is dose-dependent. Its mechanism of action may be to regulate blood lipids, reduce serum TNF-α levels.