Mechanism of Shenxiankang in Intervening Renal Fibrosis Rats Through Egulating LncRNA5318-mediated TGF-β/Smad Signal Pathway
Objective:To investigate the protective effect and mechanisms of Shenxiankang on renal fibrosis rats based on TGF-β1/Smad pathway mediated by LncRNA5318. Methods:Models of renal interstitial fibrosis in rats were established with unilat-eral urethral obstruction (UUO). Twenty-five rats were randomly divided into five groups:sham operation group,model group,benazepril group,shenxiankang low-dose and high-dose group. Corresponding drugs were given to intervene by gastric gavage in administration groups,and the same volume of normal saline was given by gastric gavage in sham surgery group and model group,Once a day for 2 consecutive weeks. Pathological changes of the renal tissue were observed by HE and Masson staining,the renal tubuloint-erstitial injury index and relative area of renal fibrosis were calculated. The protein expression levels ofα-smooth muscle actin (α-SMA),transforming growth factor-β1(TGF-β1),p-Smad2,Smad2,p-Smad3,Smad3 and Smad7 were detected by Western blot. The expression level of LncRNA5318 in kidney tissue was detected by real-time quantitative qPCR. Results:Compared with sham surgery group,obvious kidney injury and fibrosis were observed in model group. Compared with the model group,tubulointersti-tial injury index and relative area of renal fibrosis in benazepril and shenxiankang treatment groups were significantly decreased ( P<0.05). Compared with the sham operation group,the protein expression levels ofα-SMA,TGF-β1,p-Smad2 and p-Smad3 in the model group were significantly increased (P<0.05),while the expression levels of Smad7 was significantly decreased (P<0.05). Benazepril and shenxiankang could reduce the protein expression levels of α-SMA,TGF-β1,p-Smad2 and p-Smad3 and mprove the expression level of Smad7 (P<0.05). Compared with the sham operation group,the expression level of Ln-cRNA5318 in the model group was significantly increased (P<0.05),Benazepril and shenxiankang could reduce the expression level of LncRNA5318 (P<0.05). Conclusion:Shenxiankang can alleviate renal fibrosis,and its efficacy is comparable to that of benaze-pril. The mechanism may be related to the regulation of TGF-β/Smad signal pathway mediated by LncRNA5318.
ShenxiankangTGF-β/Smad signal pathwayRenal interstitial fibrosisLncRNA5318
万方数据
维普
