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目的:观察苦酸通调方对自发性糖尿病大鼠腹部脂肪组织中NF-κB及IKKβmRNA表达的影响。方法:将高脂饲料喂养的30只雄性SPF级ZDF大鼠随机分为模型对照组、苦酸通调组、吡格列酮组3组,普通饲料喂养的雄性SPF级ZL大鼠为正常对照组,每组10只。苦酸通调组根据大鼠体质量以3.29 g/(kg·d)混悬液灌胃,吡格列酮组以1.07μg/(g·d)灌胃,正常对照组和模型对照组给予等体积蒸馏水灌胃,1 d 1次,连续12周。采用RT-PCR法检测各组大鼠腹部脂肪组织中NF-κB、IKKβmRNA的表达水平。结果:模型对照组、吡格列酮组、苦酸通调组大鼠腹腔脂肪组织中NF-κB、IKKβmRNA的表达高于正常对照组,差别有统计学意义(P<0.01)。与模型对照组对比,苦酸通调组和吡格列酮组NF-κB、IKKβmRNA的表达均降低,差别有统计学意义(P<0.01,P<0.05)。与吡格列酮组对比,苦酸通调NF-κB、IKKβmRNA的表达均降低,差别有统计学意义(P<0.05)。结论:苦酸通调方在一定程度上能抑制糖尿病大鼠腹部脂肪组织中NF-κB、IKKβmRNA表达,这可能是苦酸通调方抑制炎症信号通路的传导而发挥其改善胰岛素抵抗治疗糖尿病的机制之一。
OBJECTIVE: To observe the effects of Kuisutong Recipe on the expression of NF-κB and IKKβmRNA in abdominal adipose tissue of spontaneously diabetic rats. Methods: Thirty male SPF ZDF rats fed with high-fat diet were randomly divided into three groups: model control group, moxibutone group and pioglitazone group. Normal SPF-fed ZL rats were normal control group, Group of 10. The model group was given intragastric administration of 3.29 g / (kg · d) gavage, the intragastric administration of 1.07 μg / (g · d) pioglitazone group, the normal control group and the model control group were given equal volume of distilled water Gavage, 1 d 1 times for 12 weeks. The expression of NF-κB and IKKβmRNA in abdominal adipose tissue of rats in each group were detected by RT-PCR. Results: The expressions of NF-κB and IKKβmRNA in peritoneal adipose tissue of model control group, pioglitazone group and moxibutong group were significantly higher than those of normal control group (P <0.01). Compared with the model control group, the expressions of NF-κB and IKKβmRNA in the two groups were significantly decreased (P <0.01, P <0.05). Compared with pioglitazone group, the expression of NF-κB and IKKβmRNA were down-regulated by bitterness acid, the difference was statistically significant (P <0.05). Conclusion: MTT can inhibit the expression of NF-κB and IKKβmRNA in the abdominal adipose tissue of diabetic rats, which may be due to its inhibitory effect on the inflammatory signal transduction and the improvement of insulin resistance in the treatment of diabetes One of the mechanisms.