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目的探讨参芪复方防治糖尿病大血管病变的可能分子机制。方法 160只自发性2型糖尿病GK大鼠给予高脂饲料喂养12周建立糖尿病大血管病变模型,随机分成模型组、西药组、参高组、参中组、参低组,每组32只。另设32只Wistar大鼠为空白组。造模后西药组给予二甲双胍片0.1 g/(kg·d)灌胃,参高、中、低组分别给予参芪复方2.88、1.44、0.72 g/(kg·d)灌胃,空白组和模型组给予生理盐水5 ml/(kg·d)灌胃,各组均灌胃16周。分别在给药前及给药第8、16周时检测空腹血糖;第8、16周时采用Masson染色观察胸主动脉病理形态,计算胶原纤维/血管壁面积(PVCA/LA);16周时进行差异基因筛选。结果与空白组同时间比较,模型组在给药前及给药8、16周时大鼠空腹血糖升高,第8、16周时PVCA/LA明显升高(P<0.05或P<0.01);第16周时西药组和参高、中、低组大鼠空腹血糖低于同时间模型组,PVCA/LA均显著下降(P<0.05或P<0.01)。参中组与模型组、模型组与空白组共同存在的显著性差异基因共15个,其中与糖尿病血管病变有关的基因为Elavl1、Lama4,且参中组Elavl1、Lama4基因较模型组下调。结论参芪复方防治糖尿病大血管病变作用机理可能与下调胸主动脉Elavl1、Lama4基因表达,从而抑制血管新生,减少胶原纤维产生有关。
Objective To investigate the possible molecular mechanism of Shenqi compound in prevention and treatment of diabetic macroangiopathy. Methods 160 diabetic GK rats were fed with high fat diet for 12 weeks to establish diabetic macroangiopathy model and randomly divided into model group, western medicine group, Shengao group, Shenzhong group and Shenqian low group, with 32 in each group. Another 32 Wistar rats as a blank group. The model group was given 0.1g / (kg · d) of metformin tablets orally and the high, medium and low groups were given Shenqi Compound 2.88,1.44,0.72 g / (kg · d) Groups were given saline 5 ml / (kg · d) gavage, each group were gavage for 16 weeks. Fasting blood glucose was measured before administration and at the 8th and 16th week of administration. Pathological changes of the thoracic aorta were observed by Masson staining at the 8th and 16th weeks. The area of collagen fibers / vascular wall (PVCA / LA) Differential gene screening. Results Compared with the blank group, the fasting blood glucose in model group was significantly increased at 8 and 16 weeks after administration, and at the 8th and 16th week, PVCA / LA was significantly increased (P <0.05 or P <0.01) The fasting blood glucose in the western medicine group and the high, middle and low groups were lower than those in the model group at the 16th week (P <0.05 or P <0.01). A total of 15 genes were found in the model group, the model group and the blank group. Among them, Elavl1 and Lama4 were involved in the pathogenesis of diabetes mellitus, and Elavl1 and Lama4 genes were lower than the model group. Conclusion The mechanism of Shenqi compound on the prevention and treatment of diabetic macroangiopathy may be related to the down-regulation of Elavl1 and Lama4 gene expression in the thoracic aorta, thereby inhibiting angiogenesis and reducing collagen production.