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目的:研究蜕皮甾酮对非酒精性脂肪性肝病大鼠模型肿瘤坏死因子α(TNF-α)与核因子κB(NF-κB)表达的影响,并探索其可能的作用机制。方法:健康成年SD大鼠36只,随机分为正常对照组12只与实验组24只;正常对照组喂以普通基础饲料,实验组应用高脂饲料喂养。实验12周末时将造模成功的实验组大鼠随机分为模型组与蜕皮甾酮治疗组2个亚组,每组12只;正常对照组喂以普通基础饲料至16周,模型组继续应用改良高脂饲料喂养至16周,蜕皮甾酮治疗组大鼠在高脂饮食同时加用蜕皮甾酮灌胃。实验16周末时处死3组所有大鼠;检测肝脏指数,血清与肝组织生化指标及肝组织病理改变;ELISA法检测肝脏TNF-α水平;免疫组化检测各组大鼠肝组织中核因子κB蛋白表达情况。结果:蜕皮甾酮治疗组血清胆固醇(TC)、丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)明显低于模型组(2.12±0.58比2.63±0.24,P<0.05;53.36±18.48比84.60±36.27,P<0.05;140.20±35.95比243.59±36.38,P<0.01);蜕皮甾酮治疗组与模型组相比肝组织丙二醛(MDA)水平降低明显(184.54±16.45比239.28±23.76,P<0.01),超氧化物歧化酶(SOD)活力增加显著(9.42±0.52比5.18±0.43,P<0.01),肝脏指数显著降低(4.35±0.37比5.04±0.46,P<0.01),肝组织脂肪变性程度和炎症活动度明显减轻(5.46±0.37比6.30±0.49,P<0.01)。蜕皮甾酮治疗组与模型组相比TNF-α与核因子κB水平明显减轻(43.04±7.48比61.56±7.27,24.65±5.39比45.04±7.46,P值均<0.01)。结论:蜕皮甾酮具有改善高脂饮食诱发的非酒精性脂肪性肝病大鼠肝脏酶学功能,通过增加肝组织SOD的含量和减少MDA的含量来减轻肝组织氧化应激水平,减轻肝组织TNF-α和核因子κB来减轻肝脏炎症,发挥防治非酒精性脂肪性肝病的作用。
Objective: To study the effect of ecdysterone on the expression of tumor necrosis factor-α (TNF-α) and nuclear factor-κB (NF-κB) in rat models of non-alcoholic fatty liver disease, and to explore its possible mechanism. Methods: Thirty-six healthy adult SD rats were randomly divided into 12 normal control groups and 24 experimental groups. The normal control group was fed with basic basal diet and the experimental group was fed with high fat diet. At the end of the experiment, the rats in the experimental group were randomly divided into two subgroups: the model group and the ecdysterone treatment group, 12 in each group. The normal control group was fed with the basic basal diet for 16 weeks, and the model group continued to be used. The modified high-fat diet was fed for 16 weeks. The ecdysterone-treated group rats were given intragastric administration of ecdysterone at the same time on a high-fat diet. All rats in the 3 groups were sacrificed at the end of the 16th week of the experiment. Liver index, serum and hepatic tissue biochemical indexes and liver pathological changes were detected. ELISA was used to detect the level of hepatic TNF-α. Immunohistochemistry was used to detect the NF-κB protein in the liver of rats in each group. Expression of situation. Results: Serum cholesterol (TC), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly lower in the ecdysterone treatment group than in the model group (2.12±0.58 vs 2.63±0.24, P<0.05). 53.36±18.48 vs. 84.60±36.27, P<0.05; 140.20±35.95 vs. 243.95±36.38, P<0.01); MDA levels in the ecdysterone-treated group decreased significantly compared with the model group (184.54± 16.45 vs. 239.28±23.76, P<0.01), superoxide dismutase (SOD) activity increased significantly (9.42±0.52 vs 5.18±0.43, P<0.01), liver index decreased significantly (4.35±0.37 vs 5.04±0.46, P <0.01), the degree of steatosis and inflammatory activity in hepatic tissue was significantly reduced (5.46±0.37 vs 6.30±0.49, P<0.01). Compared with the model group, the TNF-α and NF-κB levels were significantly reduced in the ecdysterone treatment group (43.04±7.48 vs. 61.56±7.27, 24.65±5.39 vs. 45.04±7.46, P<0.01). Conclusion:Ecdysterone can improve the hepatic enzymology of rats with non-alcoholic fatty liver disease induced by high-fat diet. It can reduce the liver oxidative stress and liver tissue TNF by increasing the content of SOD and reducing the content of MDA. -α and nuclear factor kappa B to reduce liver inflammation, play a role in the prevention and treatment of non-alcoholic fatty liver disease.