基于ACE/AngⅡ/AT1R通路探讨补肾降压方对盐敏感性高血压大鼠肾纤维化的作用机制OA北大核心CHSSCDCSTPCD

Objective:To investigate the regulatory effects of Bushen Jiangya Prescription on renal fibrosis and the angiotensin-con-verting enzyme(ACE)-angiotensin Ⅱ(Ang Ⅱ)-angiotensin Ⅱ type 1 receptor(AT1R)signaling pathway in salt-sensitive(DS)hy-pertensive rats and explore the mechanism of this prescription in preventing and treating hypertensive renal damage.Methods:For-ty-eight DS hypertensive rats were randomized into low salt(LS),high salt(HS),valsartan(Va),and Bushen Jiangya Prescription(BS)groups.The rats were fed with the diets containing different concentrations of sodium and then administrated with correspond-ing drugs for 8 weeks.Blood pressure was measured before and after treatment.The serum levels of creatinine(Cr),blood urea ni-trogen(BUN),Ang Ⅱ,and transforming growth factor-β,(TGF-β1)were determined by enzyme-linked immunosorbent assay(ELISA)after treatment.Hematoxylin-eosin staining and Masson staining were employed to observe the pathological changes and fibrosis degree,respectively,in the renal tissue.The mRNA and protein levels of ACE and AT1R in the renal tissue were measured by reverse transcription polymerase chain reaction(RT-PCR)and Western blotting,respectively.Results:After the rats were fed with the diets containing different concentrations of salt for 3 weeks,the systolic blood pressure in the groups fed with high salt was higher than that in the LS group(P＜0.01).After treatment,compared with the LS group,the HS group showcased elevated systolic blood pressure and levels of Cr,BUN,Ang Ⅱ,and TGF-β1,severe renal fibrosis,and up-regulated protein and mRNA levels of ACE and AT1R in the renal tissue(P＜0.01).Compared with the HS group,the Va and BS groups showed lowered systolic blood pres-sure and levels of Scr,BUN,Ang Ⅱ,and TGF-β1,alleviated renal fibrosis,and down-regulated protein and mRNA levels of ACE and AT1R in the renal tissue(P＜0.05,P＜0.01).Conclusion:Bushen Jiangya Prescription exerts the effects of lowering hyper-tension and improving the renal function by regulating the ACE/Ang Ⅱ/AT1R axis and inhibiting TGF-β1 to mitigate renal fibrosis.