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作 者:周燕萍 周姝含 吕文亮 孙易娜 王上 柳志成 ZHOU Yan-ping;ZHOU Shu-han;LU Wen-liang;SUN Yi-na;WANG Shang;LIU zhi-cheng(Hubei University of Chinese Medicine,Wuhan Hubei 430061,China)
机构地区:[1]湖北中医药大学中医临床学院,湖北武汉430061
出 处:《时珍国医国药》2018年第10期2362-2364,共3页Lishizhen Medicine and Materia Medica Research
基 金:湖北省自然科学基金面上项目(2016CFB635)
摘 要:目的观察王氏连朴饮加味方对糖尿病大鼠血清CRP、TNF-α、IL-6及血脂的影响,探讨此方对改善胰岛素抵抗的作用机理。方法雄性SD大鼠经高糖高脂饲料饲喂6周,注射STZ,3天后禁食过夜,检测大鼠空腹血糖浓度≥16. 67mmol/L者为造模成功大鼠,随机分为模型对照组、阿司匹林组和王氏连朴饮加味方组共3组,并另设正常大鼠对照组。给药组按6g/(kg·d)灌服王氏连朴饮加味方;阿司匹林组按120 mg/(kg·d)灌服阿司匹林混悬液;模型对照组和正常对照组灌服等容量蒸馏水,连续灌胃治疗8周。测定大鼠血清CRP和TNF-α、IL-6含量及血脂、血糖、和胰岛素水平、并计算胰岛素敏感指数。结果王氏连朴饮加味方及阿司匹林均能显著降低血清TNF-α、CRP、IL-6含量以及TC、TG、FFA含量,显著降低空腹血糖和血清胰岛素水平,胰岛素敏感性增强。且王氏连朴饮加味方在降低血清TG含量以及空腹血糖方面优于阿司匹林组(P <0. 01)。结论王氏连朴饮加味方能抑制糖尿病大鼠炎症因子释放,纠正脂质代谢紊乱,降低胰岛素抵抗的发生风险。炎症因子可能是胰岛素抵抗发生的致病介质,参与Ⅱ型糖尿病的发生机制,增加胰岛素抵抗的发生风险,而血脂异常可能通过刺激炎症因子的产生而共同参与胰岛素抵抗,可为临床治疗提供新的思路。Objective To observe the effect of the modified Wang’s lianpu decoction(WLPD) on diabetic rats serum CRP,TNF-α,IL-6,and the blood lipids,to study the mechanism of the decoction to improve the insulin resistance. Methods Male SD rats by high sugar and high fat feedstuff feeding for 6 weeks,STZ injection,three days after fasting overnight,detection of fasting blood glucose levels in rats,higher than 16. 67 mmol/L for building successful model,were randomly divided into model control group,aspirin group and the modified WLPD group,a total of 3 groups,and a normal rats in control group. The administration group was given modified WLPD by 6 g/(kg· d). Aspirin suspension was administered in the aspirin group at 120 mg/(kg·d). Model control group and normal control group were given distilled water of equal capacity,orally 8 weeks. Serum CRP and TNF-α、IL-6 and the blood lipids、insulin levels were measured. Results The modified WLPD and aspirin can significantly reduce serum TNF-α,CRP,IL-6 levels and the results of TC,TG,FFA,significantly reduced fasting blood glucose and serum insulin levels,and enhanced insulin sensitivity. Moreover,there was a statistically significant difference in serum TG and fasting glucose between the two groups(P < 0. 01). Conclusion The modified WLPD can inhibit the release of inflammatory factors in diabetic rats,correct the disorder of lipid metabolism and reduce the risk of insulin resistance. Inflammatory factors may be the disease-causing agents for insulin resistance,involved in the mechanism of T2 DM and increases the risk of the occurrence of insulin resistance. Dyslipidemia may co-participate in insulin resistance by stimulating the production of inflammatory cytokines and this can provide new ideas for clinical treatment.
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