目的:探讨脾虚痰浊动脉硬化(AS)巴马小型猪肾组织水通道蛋白的改变及益气健脾法的干预作用及机制.方法:将15只巴马小型猪随机分为正常组、模型组(脾虚痰浊AS模型)、益气健脾组各5只,以高脂饮食喂饲加跑步劳倦结合冠脉球囊拉伤建立脾虚痰浊AS模型.正常组巴马小型猪喂饲正常饲料,模型组球囊冠脉拉伤后高脂饲料结合跑步过劳制备脾虚痰浊AS模型,益气健脾组在模型组处理基础上于高脂饲料中添加益气健脾中药,观察48周后各组巴马小猪的肾脏组织病理形态学改变,肾组织环磷酸腺苷(cAMP)含量、水通道蛋白(AQP)1、2、3及磷酸化蛋白激酶A(p-PKA)、磷酸化cAMP反应原件结合蛋白(p-CREB)表达变化.结果:与正常组比较模型组肾组织病理形态学可见肾小球及肾小管损伤,肾组织AQP1、2、3下调,cAMP/PKA/CREB通路下调,与模型组比较益气健脾组可上调肾组织AQP1、2、3及cAMP/PKA通路.结论:脾虚痰浊AS模型可见肾组织病理损伤,肾组织AQP1、2、3下调,益气健脾法可改善肾组织病理损伤,上调脾虚痰浊AS模型肾脏水通道蛋白的异常,其机制可能与调节cAMP/PKA通路相关.%Object:To observe the changes of kidney water channel protein and cAMP/PKA signal pathway with the spleen dificiency and phlegm atherosclerosis bana mini-pig model and effect of the replenishing spleen on the model.Method:Fifteen bama minipigs were randomly divided into normal group,model group and replenishing spleen group with five in each.The spleen dificiency and phlegm atherosclerosis model were instant by high fat diet combined tied by running after balloon injury in the coronary artery.The bama minipigs of normal group were fed normal basic diet for 48 weeks,model group were fed high fat and high calorie fodder for 48 weeks.The bana mini-pigs of replenishing spleen group were gived replenishing spleen recipe on the basis of the method on model group after 24 weeks.Observing Cyclic adenosine monophosphate(cAMP) 、morphology and the protein expression of aquaporins (AQP)1、2、3 、phosphorylation protein kinase A(p-PKA) 、phosphorylated cAMP-response element binding protein (p-CREB) in the mini-pigs kidney after 48weeks.Result:Compared with normal group,morphology of kidney of the model group show the pathological damage in the glomerular and tubular,expression of AQP1、2、3 and cAMP/PKA/CREB pathway were reduced.Compared with normal group,replenishing spleen group increased expression of AQP1、2、3 and cAMP/PKA pathway in the bama mini-pigs kidney.Conclusion:Spleen deficienly and phlegm atherosclerosis model show morphology of the kidney and decrease of AQP1,2,3,methods for replenishing spleen can regulate abnormal water metabolism regulatory proteins,possibly related to cAMP/PKA pathway.
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