蚕蛹油对高脂高糖诱导大鼠脂肪性肝炎的治疗作用研究

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目的:观察蚕蛹油对高脂高糖诱发脂肪性肝炎的治疗作用,并探讨其可能的机制。方法:雄性清洁级SD大鼠随机分为正常组、模型组、蚕蛹油1.8mg/kg组,蚕蛹油3.6mg/kg组和阳性药罗格列酮4mg/kg组。在用高脂高糖乳剂造成脂肪性肝炎后,给药组大鼠分别灌服蚕蛹油或罗格列酮,连续4周,然后取血测定大鼠血清总胆固醇(TC)、甘油三酯(TG)、游离脂肪酸(FFA)、谷丙转氨酶(ALT)和谷草转氨酶(AST)含量,取肝组织称重并计算肝重系数,同时测定肝组织中TC、TG和还原型谷胱甘肽(GSH)含量以及超氧化物歧化酶(SOD)的活性,光镜检查肝组织的形态学改变。另外,采用RT-PCR法测定肝组织中肿瘤坏死因子(TNF)α和过氧化物酶体增生物激活受体(PPAR)γmRNA表达。结果:脂肪性肝炎大鼠给予蚕蛹油1.8mg/kg和3.6mg/kg治疗4周后,对血中TC、TG、FFA和ALT含量有明显的降低作用,蚕蛹油3.6mg/kg组对肝组织中的TG含量也有降低作用,但未见对肝组织中TC含量有明显的影响。与模型组比较,蚕蛹油组的血清AST含量,以及肝重系数和肝中SOD活性未见有明显的改变,但蚕蛹油3.6mg/kg能明显增加大鼠肝组织中的GSH含量。光镜下可见,给予蚕蛹油治疗后的大鼠肝脏脂质空泡有一定的改善作用,而炎性细胞的浸润则明显减少,尤以蚕蛹油3.6mg/kg组的作用更好。另外,RT-PCR实验结果显示,蚕蛹油能够明显降低高脂饮食大鼠肝组织TNF-αmRNA表达,而同时增加PPARγmRNA表达。结论:蚕蛹油能治疗高脂高糖诱导的大鼠脂肪性肝炎,其作用机制可能与调节脂代谢,抗氧化,以及通过增加PPARγ表达而降低炎性细胞因子TNF-α表达有关。 Objective: To observe the therapeutic effect of silkworm pupa oil on steatohepatitis induced by high fat and high glucose, and to explore its possible mechanism. Methods: Male SD rats were randomly divided into normal group, model group, 1.8 mg / kg silkworm pupa oil group, 3.6 mg / kg silkworm pupa oil and 4 mg / kg rosiglitazone group. After steatohepatitis was induced by high-fat and high-sucrose emulsion, the rats in the treatment group were fed with silkworm pupa oil or rosiglitazone respectively for 4 weeks, then the blood samples were taken for determination of serum total cholesterol (TC), triglyceride (TG), free fatty acid (FFA), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured. The liver tissue was weighed and the hepatic weight coefficient was calculated. The contents of TC, TG and reduced glutathione GSH) content and superoxide dismutase (SOD) activity, light microscopy liver morphology changes. In addition, the mRNA expression of tumor necrosis factor (TNF) alpha and peroxisome proliferator-activated receptor (PPAR) in liver tissue was determined by RT-PCR. Results: After treatment with 1.8 mg / kg and 3.6 mg / kg silkworm pupa oil for 4 weeks, the levels of TC, TG, FFA and ALT in blood of the rats with steatohepatitis were significantly decreased. Tissue TG content also decreased, but no significant effect on liver tissue TC content. Compared with the model group, there was no obvious change in serum AST, hepatic weight index and SOD activity in the liver of the pupae oil group. However, the GSH content in the rat liver tissue was significantly increased by the pupa oil 3.6mg / kg. Light microscopy shows that the administration of pupae oil treated rat liver lipid vacuoles have a certain degree of improvement, while the infiltration of inflammatory cells was significantly reduced, especially in the role of pupa oil 3.6mg / kg group better. In addition, the results of RT-PCR showed that the silkworm pupae oil significantly decreased the expression of TNF-αmRNA and increased the expression of PPARγmRNA in the liver of the high-fat diet rats. CONCLUSION: Silkworm pupa oil can treat steatohepatitis induced by high-fat and high-glucose in rats. The mechanism may be related to the regulation of lipid metabolism, antioxidation and the decrease of inflammatory cytokine TNF-α expression by increasing PPARγ expression.
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