摘要
[Objectives]To study the protective effects of Manshenkangning Prescription on adenine-induced renal interstitial fibrosis in rats,and explore the possible mechanism.[Methods]Sixty Wistar male rats were divided into normal group,model group,control group(administered with 10 mg/(kg·d)losartan)and high,medium and low dose experimental groups(30,15,7.5 mg/(kg·d)Manshenkangning).The rat models of renal interstitial fibrosis were induced by intragastric administration of adenine(250 mg/(kg·d)).After 2 h,the above drugs were administered intragastrically for 21 consecutive days and the administration time was 30 consecutive days.Serum creatinine(SCr),blood urea nitrogen(BUN),24 h urinary protein(24 h MTP)and glomerular filtration rate(eGFR)were measured by biochemical method;renal histopathological changes were observed by hematoxylin-eosin(HE)staining.Renal collagen deposition in rats was observed by Masson staining.[Results]The SCr in model group and the high,medium and low dose experimental groups were(340.00±22.99),(176.80±18.60),(234.75±13.59),(266.11±14.78)μmol/L,and BUN were(23.74±2.51),(14.53±2.25),(18.78±0.88),(18.90±2.14)mmol/L;24 h MTP were(675.86±74.58),(323.81±41.83),(438.84±34.69),(493.76±37.04)mg/d;eGFR were(19.30±2.48),(49.96±10.95),(32.61±10.75),(27.18±5.98)mL/min,and the difference was statistically significant compared with the normal group(all P<0.05).HE staining and Masson staining showed that compared with normal group,the renal interstitial lesions in model group were severe and the renal interstitial collagen material was deposited in a large amount.The renal interstitial tubule injury was relieved and the renal interstitial collagen deposition was reduced in experimental groups.And the difference was statistically significant(all P<0.01).[Conclusions]Manshenkangning can significantly protect the kidney against the progress of interstitial fibrosis in rats.Its possible mechanism is to regulate the activity of SIRT1 and inhibit the expression of COX-2 in order to resist the inflammatory reaction of kidney and improve the ability of anti-oxidative stress of kidney,thus delaying the occurrence and development of chronic renal failure.
[Objectives] To study the protective effects of Manshenkangning Prescription on adenine-induced renal interstitial fibrosis in rats, and explore the possible mechanism. [Methods] Sixty Wistar male rats were divided into normal group, model group, control group(administered with 10 mg/(kg·d) losartan) and high, medium and low dose experimental groups(30, 15, 7.5 mg/(kg·d) Manshenkangning). The rat models of renal interstitial fibrosis were induced by intragastric administration of adenine(250 mg/(kg·d)). After 2 h, the above drugs were administered intragastrically for 21 consecutive days and the administration time was 30 consecutive days. Serum creatinine(SCr), blood urea nitrogen(BUN), 24 h urinary protein(24 h MTP) and glomerular filtration rate(eGFR) were measured by biochemical method; renal histopathological changes were observed by hematoxylin-eosin(HE) staining. Renal collagen deposition in rats was observed by Masson staining. [Results] The SCr in model group and the high, medium and low dose experimental groups were(340.00±22.99),(176.80±18.60),(234.75±13.59),(266.11±14.78) μmol/L, and BUN were(23.74±2.51),(14.53±2.25),(18.78±0.88),(18.90±2.14) mmol/L; 24 h MTP were(675.86±74.58),(323.81±41.83),(438.84±34.69),(493.76±37.04) mg/d; eGFR were(19.30±2.48),(49.96±10.95),(32.61±10.75),(27.18±5.98) mL/min, and the difference was statistically significant compared with the normal group(all P<0.05). HE staining and Masson staining showed that compared with normal group, the renal interstitial lesions in model group were severe and the renal interstitial collagen material was deposited in a large amount. The renal interstitial tubule injury was relieved and the renal interstitial collagen deposition was reduced in experimental groups. And the difference was statistically significant(all P<0.01). [Conclusions] Manshenkangning can significantly protect the kidney against the progress of interstitial fibrosis in rats. Its possible mechanism is to regulate the activity of SIRT1 and inhibit the expression of COX-2 in order to resist the inflammatory reaction of kidney and improve the ability of anti-oxidative stress of kidney, thus delaying the occurrence and development of chronic renal failure.
基金
Supported by Supported by the Scientific Research Foundation Project of Traditional Chinese Medicine Bureau of Guangdong Province(20171075,20191093).
作者简介
Corresponding author:Long YI,E-mail:yilong_shh@163.com;Corresponding author:Shiping ZHU,E-mail:gzjnuzsp@163.com
