Hydrogen sulfide inhibits the renal fibrosis of chronic kidney disease

4^th International Conference on Nephrology & Therapeutics

September 14-16, 2015 Baltimore, USA

Kai Song

Soochow University, China

Posters-Accepted Abstracts: J Nephrol Ther

Abstract :

Hydrogen sulfide (H2S) represents the third gasotransmitter along with nitric oxide and carbon monoxide. Recently it has been found that H2S levels were decreased in chronic kidney disease but its physiological functions in kidney have not been fully elucidated. Previous work demonstrates that H2S has diuretic, natriuretic and kaliuretic properties. It can also increase glomerular filtration rate and functions as an oxygen sensor in the renal medulla. Using the rat model of unilateral ureteral obstruction, we verified that cystathionine-�²-synthase was the dominant H2S-producing enzyme located in renal tubular while another H2S-generating enzyme cystathionine-�³-lyase was mainly expressed in glomeruli. Administration with 56 �¼g/kg.d sodium hydrogen sulfide (a H2S donor) inhibited renal fibrosis by attenuating the production of collagen, extracellular matrix and the expression of a-smooth muscle actin. The underlying mechanisms were associated with the anti-inflammation effect of H2S as well as its anti-proliferative and antidifferentiation properties on renal fibroblasts. Using a rate model of peritoneal fibrosis, our current data also confirmed that H2S was able to improve the peritoneal function and inhibits peritoneal fibrosis caused by peritoneal dialysis solution. Thus, low doses of H2S or its releasing compounds may have therapeutic potentials in treating chronic kidney disease.

Biography :

Email: songkaift3@live.cn