scholarly journals Podocyte-specific soluble epoxide hydrolase deficiency in mice attenuates acute kidney injury

FEBS Journal ◽  
2017 ◽  
Vol 284 (13) ◽  
pp. 1970-1986 ◽  
Author(s):  
Ahmed Bettaieb ◽  
Shinichiro Koike ◽  
Samah Chahed ◽  
Yi Zhao ◽  
Santana Bachaalany ◽  
...  
2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Chin-Wei Chiang ◽  
Hsueh-Te Lee ◽  
Der-Cherng Tarng ◽  
Ko-Lin Kuo ◽  
Li-Ching Cheng ◽  
...  

Soluble epoxide hydrolase (sEH) is abundantly expressed in kidney and plays a potent role in regulating inflammatory response in inflammatory diseases. However, the role of sEH in progression of chronic kidney diseases such as obstructive nephropathy is still elusive. In current study, wild-type (WT) andsEHdeficient (sEH−/−) mice were subjected to the unilateral ureteral obstruction (UUO) surgery and the kidney injury was evaluated by histological examination, western blotting, and ELISA. The protein level of sEH in kidney was increased in UUO-treated mice group compared to nonobstructed group. Additionally, UUO-induced hydronephrosis, renal tubular injury, inflammation, and fibrosis were ameliorated insEH−/−mice with the exception of glomerulosclerosis. Moreover,sEH−/−mice with UUO showed lower levels of inflammation-related and fibrosis-related protein such as monocyte chemoattractant protein-1, macrophage inflammatory protein-2, interleukin-1β(IL-1β), IL-6, inducible nitric oxide synthase, collagen 1A1, andα-actin. The levels of superoxide anion radical and hydrogen peroxide as well as NADPH oxidase activity were also decreased in UUO kidneys ofsEH−/−mice compared to that observed in WT mice. Collectively, our findings suggest that sEH plays an important role in the pathogenesis of experimental obstructive nephropathy and may be a therapeutic target for the treatment of obstructive nephropathy-related diseases.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Dinesh Kumar Patel ◽  
Kanika Patel

Abstract Background and Aims Oxidative stress and inflammation is the major contributor of kidney injury and the drugs which have antioxidant and anti-inflammatory activity could protect kidney against renal damage. Mechanisms involved in renal failure include oxidative stress, inflammation and apoptosis which lead myoglobinemia, myoglobinuria and cast formation. Inflammatory mediators such as IL-1, ICAM-1 and TNFα also play important role in renal failure. Excess production of uric acid can cause serious consequence in hyperuricemia and xanthine oxidase (XO) catalyzes the oxidation of xanthine to uric acid. Protective effects of gossypetin in the management of kidney injury and related disorders have been investigated in the present work through inhibitory potential of gossypetin on nuclear factor kappa B (NF-κB), soluble epoxide hydrolase (sEH) and XO. Method Present work described the medicinal importance of gossypetin with their beneficial effect on kidney disorder. In-silico molecular docking and dynamic experiments were carried out with gossypetin against nuclear factor kappa B (NF-κB) and soluble epoxide hydrolase (sEH). Further docking was also performed to investigate how gossypetin and the active site of XO fit together. Results From the analysis of the available data’s in the present work, it was found that gossypetin have protective effect against nephrotoxicity. Gossypetin also showed potent anti-inflammatory activity in kidney mesangial cells which further support application of natural compounds on nephritis treatment. Importance of gossypetin for preventing renal damage has been also emphasized due to its antioxidants potential. In-silico studies showed that, gossypetin exhibited a higher docking score against NF-κB and sEH. Docking studies revealed gossypetin surrounds the active sites of XO and reduces conversion of xanthine to uric acid. Conclusion Study revealed their antioxidant, anti-mutagenic, anti-atherosclerotic, anti-microbial and cytoprotective properties. The protective effect of gossypetin in kidney could be due to its antioxidant and anti-inflammatory activity through inhibition of NF-κB and sEH upregulation.


Sign in / Sign up

Export Citation Format

Share Document