金锁固精丸加味通过调控Podocin/Nephrin和整合素表达减轻糖尿病肾病足细胞损伤的机制研究OA

Objective:To observe the effect of Modified Jinsuo Gujing Pills(MJGP)on podocyte injury in diabetic nephropathy(DN)rats and to explore its mechanism by regulating the expression of key podocyte proteins,Podocin,Nephrin,and integrins α3 and β1.Methods:Thirty-six clean-grade male Sprague-Dawley(SD)rats were randomly divided into a normal group(n=6),a model control group(n=15),and a Modified Jinsuo Gujing Pills intervention group(n=15).The DN model was induced by intraperitoneal injection of streptozotocin(STZ).One week after successful modeling,the intervention group received Modified Jinsuo Gujing Pills granule suspension by gavage,while the normal and model groups received an equal volume of normal saline for 12 consecutive weeks.Blood glucose,24-hour urinary protein,and urinary podocyte count were dynamically monitored at the 4th and 12th weeks.After treatment,rats were sacrificed,and renal cortex tissues were collected.The mRNA expression levels of Podocin,Nephrin,and integrins α3 and β1 were detected by real-time quantitative polymerase chain reaction(qPCR).Results:After 12 weeks of intervention,compared with the model group,the intervention group showed significantly lower blood glucose levels(P<0.01),significantly reduced 24-hour urinary protein excretion and urinary podocyte count(both P<0.01).Concurrently,the mRNA expression levels of Podocin,Nephrin,integrin α3,and integrin β1 in the renal cortex of the intervention group were significantly increased compared to the model group(all P<0.01).The mRNA expression levels of these molecules in the model group were significantly lower than those in the normal group(all P<0.01).Conclusion:Modified Jinsuo Gujing Pills can lower blood glucose,reduce proteinuria and urinary podocyte excretion in DN rats.The mechanism may be related to upregulating the mRNA expression of key slit diaphragm proteins(Podocin,Nephrin)and adhesion molecules(integrins α3,β1)in podocytes,thereby protecting podocytes and alleviating injury.