AIMS: To investigate the protective effects of exogenous hydrogen sulfide (H2 S) against unilateral ureteric obstruction (UUO) induced renal injury and explore the potential mechanisms involved. METHODS: Rats were randomly divided into four groups: sham group, UUO group, UUO + saline group, and UUO + NaHS group. Rats were sacrificed on Day 10 after UUO. The tubulointerstitial injury, interstitial fibrosis, and the infiltrating of macrophages in the interstitium were assessed. Expression of TNF-α in kidney tissue was also measured. Oxidative stress was evaluated by detecting the level of MDA and SOD in renal tissues. RESULTS: Interstitial fibrosis and renal injury score were markedly increased on Day 10 after UUO. In contrast, administration of NaHS significantly reduced the injury score. In addition, the kidneys that were treated with NaHS exhibited minimal interstitial fibrosis. The number of ED1 positive cells in the interstitium and the level of TNF-α were significantly higher in UUO kidneys compared with that in sham group. NaHS treatment significantly attenuated infiltration of macrophages and the expression of TNF-α. Our findings showed a significant increase in MDA level and decrease in the SOD activity in the UUO group compared to the sham group. However, significant decrease in MDA level and increase in SOD activity were observed after treatment of NaHS. CONCLUSIONS: Our study demonstrates that NaHS protects against UUO-induced renal damage via attenuating fibrosis, oxidative stress, and inflammation. Therefore, H2 S may be useful as a potential candidate in the treatment of renal damage induced by obstruction. Neurourol. Urodynam. 33:538-543, 2014.
AIMS: To investigate the protective effects of exogenous hydrogen sulfide (H2 S) against unilateral ureteric obstruction (UUO) induced renal injury and explore the potential mechanisms involved. METHODS:Rats were randomly divided into four groups: sham group, UUO group, UUO + saline group, and UUO + NaHS group. Rats were sacrificed on Day 10 after UUO. The tubulointerstitial injury, interstitial fibrosis, and the infiltrating of macrophages in the interstitium were assessed. Expression of TNF-α in kidney tissue was also measured. Oxidative stress was evaluated by detecting the level of MDA and SOD in renal tissues. RESULTS:Interstitial fibrosis and renal injury score were markedly increased on Day 10 after UUO. In contrast, administration of NaHS significantly reduced the injury score. In addition, the kidneys that were treated with NaHS exhibited minimal interstitial fibrosis. The number of ED1 positive cells in the interstitium and the level of TNF-α were significantly higher in UUOkidneys compared with that in sham group. NaHS treatment significantly attenuated infiltration of macrophages and the expression of TNF-α. Our findings showed a significant increase in MDA level and decrease in the SOD activity in the UUO group compared to the sham group. However, significant decrease in MDA level and increase in SOD activity were observed after treatment of NaHS. CONCLUSIONS: Our study demonstrates that NaHS protects against UUO-induced renal damage via attenuating fibrosis, oxidative stress, and inflammation. Therefore, H2 S may be useful as a potential candidate in the treatment of renal damage induced by obstruction. Neurourol. Urodynam. 33:538-543, 2014.