Journal
BRAZILIAN ARCHIVES OF BIOLOGY AND TECHNOLOGY
Volume 59, Issue -, Pages -Publisher
INST TECNOLOGIA PARANA
DOI: 10.1590/1678-4324-2016150622
Keywords
hypoxia; arginine; carnosine; inflammatory molecules; renal damage
Categories
Funding
- Research Center of the Center for Female Scientific and Medical Colleges, Deanship of Scientific Research, King Saud University
Ask authors/readers for more resources
This study aimed to explore the effective role of carnosine and /or L-arginine in down regulation of the inflammatory molecule expression caused renal damage in response to sodium nitrite (NaNO2) induced hypoxia in rats. NaNO2 was administered subcutaneously (s.c.) to rats as a single dose (60 mg/kg body weight). L-arginine (200mg/Kg body weight) and carnosine (250 mg/Kg body weight) were administered (i.p.) as a single dose, 24 h before NaNO2 injection. The results revealed that preadministration of arginine and /or carnosine to NaNO2 hypoxic rats, significantly modulated the increases in serum markers of renal function (creatinine and urea) as well as the decrease in hemoglobin (Hb) level versus hypoxic rats. The two agents each alone or in a combination, markedly down regulated the serum pro-inflammatory molecules, including tumor necrosis factor-alpha (TNF-alpha), Creactive protein (CRP), vascular endothelial growth factor (VEGF) and heat shock protein -70 (HSP-70) as well as interleukin-6 (IL-6) in renal tissue compared to NaNO2 hypoxic rats. Also, the two agents successfully down modulated the alteration in the serum hypoxia inducible factor 1 alpha (HIF 1 alpha). The present biochemical results were also supported by histopathological examination. In conclusion, the current data revealed that although the efficacy of arginine or carnosine each alone, their combination was more effective in ameliorating the renal damage induced by inflammatory molecules in response to NaNO2 hypoxia. This may support the use of this combination as an effective drug to treat hypoxic renal damage
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available