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目的探讨参芪复方对2型糖尿病骨骼肌损害的影响及可能作用机制。方法 18只自发性2型糖尿病(GK)大鼠随机分为模型组、参芪复方组及西格列汀组,每组6只;另设Wistar大鼠6只为正常对照组。除正常对照组外,其余各组给予高脂饮食连续8周建立2型糖尿病模型。造模同时正常对照组、模型组均按5 ml/(kg·d)给予生理盐水灌胃,参芪复方组按1.44 g/(kg·d)给予参芪复方浸膏灌胃,西格列汀组按16 mg/(kg·d)给予磷酸西格列汀片混悬液灌胃。试验结束后检测各组大鼠血清胰岛素样生长因子1(IGF-1)、肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)含量,取腓肠肌称取湿重并观察其病理形态学改变,检测腓肠肌p70s6k1蛋白表达。结果与正常对照组比较,模型组大鼠腓肠肌湿重、血清IGF-1水平及p70s6k1蛋白明显降低(P<0.05),血清TNF-α、IL-1β含量明显升高(P<0.05),且病理观察发现腓肠肌细胞萎缩,有较大面积水肿,肌间淋巴细胞浸润。与模型组比较,西格列汀组及参芪复方组大鼠腓肠肌湿重、IGF-1含量及p70s6k蛋白表达均明显升高,TNF-α、IL-1β含量明显降低(P<0.05),且病理观察未见明显肌细胞萎缩、水肿,炎细胞浸润少。西格列汀组与参芪复方组各指标比较,差异均无统计学意义(P>0.05)。结论参芪复方可减轻糖尿病骨骼肌损害,其可能机制是减少炎性因子含量,升高血清IGF-1水平,从而维持骨骼肌质量。
Objective To investigate the effect of Shenqi Compound on skeletal muscle damage in type 2 diabetic rats and its possible mechanism. Methods 18 spontaneously diabetic rats were randomly divided into model group, Shenqi compound group and sitagliptin group, with 6 rats in each group. Six other Wistar rats were selected as normal control group. In addition to the normal control group, the remaining groups were given high-fat diet for 8 weeks to establish type 2 diabetes model. At the same time, the normal control group and the model group were intragastrically given 5 ml / (kg · d) saline, while the Shenqi Compound group was given Shenqi Compound Extract orally at the dosage of 1.44 g / (kg · d) In the statin group, sitagliptin phosphate tablets were given intragastrically at a dose of 16 mg / (kg · d). After the test, the levels of serum insulin-like growth factor 1 (IGF-1), tumor necrosis factor alpha (TNF-alpha) and interleukin 1 beta (IL-1beta) were detected in each group. Pathological changes, gastrocnemius muscle p70s6k1 protein expression. Results Compared with the normal control group, the gastrocnemius muscle wet weight, serum IGF-1 level and p70s6k1 protein in the model group were significantly decreased (P <0.05), and the levels of TNF-α and IL-1β in the model group were significantly increased Pathological observation showed gastrocnemius cells atrophy, a larger area of edema, interstitial lymphocyte infiltration. Compared with model group, gastrocnemius wet weight, IGF-1 content and p70s6k protein expression in sitagliptin group and Shenqi compound group were significantly increased, and TNF-α and IL-1β levels were significantly decreased (P <0.05) No significant muscle cell atrophy, edema and inflammatory cell infiltration were observed in pathological examination. There was no significant difference in each index between sitagliptin group and Shenqi compound group (P> 0.05). Conclusion Shenqi Compound can reduce the damage of skeletal muscle of diabetic rats. Its possible mechanism is to reduce the content of inflammatory factors, raise the level of serum IGF-1 and maintain the skeletal muscle mass.