American Journal of Infectious Diseases

Protective Effect of Enicostemma littorale Blume Methanolic Extract on Gentamicin-Induced Nephrotoxicity in Rats

Niraj M. Bhatt, Kinjal Chauhan, Sharad Gupta, Prakash Pillai, Chirayu Pandya, Jyoti V. Thaikoottathil and Sarita S. Gupta

DOI : 10.3844/ajidsp.2011.83.90

American Journal of Infectious Diseases

Volume 7, Issue 4

Pages 83-90

Abstract

Problem statement: The Amino glycoside antibiotics cause drug induced nephrotoxicity at therapeutic doses and thus limits the use clinically. Oxidative stress is one of the main reasons for the development of nephrotoxicity. Approach: In light of this the aim of the present study was to investigate the role of mitochondrial as well as post-mitochondrial oxidative stress in the development of Gentamicin (GM) induced nephrotoxicity and to elucidate the role of Enicostemma Littoral blame (EL) extract, as a promising antioxidant therapy. Rats were divided into four groups, 1) (Control 2) GM (i.p., 80 mg kg<sup>-1</sup> day<sup>-1</sup> for 8 days) (treated 3) GM+EL treated (i.g, 2.5 gm kg<sup>-1</sup> day<sup>-1</sup>) and (4) GM+ Vitamin C (VC) treated (i.g, 600 mg kg<sup>-1</sup> day<sup>-1</sup>). GM treated animals showed high oxidative stress in mitochondrial as well as post-mitochondrial fractions of renal tissues as evidenced by increased lipid per oxidation levels, decrease in GSH content and activities of antioxidant enzymes, SOD and GPx. Results: Oxidative stress was more pronounced in mitochondrial fraction as compared to post-mitochondrial fraction. GM-induced nephrotoxicity was further corroborated by an increase in serum cretonne and Blood Urea Nitrogen (BUN) levels and altered kidney histopathological observations. Treatment with EL ameliorates antioxidant defense system of mitochondrial as well as post-mitochondrial fraction, with better improvement seen in mitochondrial fraction. Conclusion: The present study explored beneficial effect of EL extract as an antioxidant therapy to counteract mitochondrial and post-mitochondrial oxidative stress generated in kidney upon GM-treatment, thus prevented nephrotoxicity.

Copyright

© 2011 Niraj M. Bhatt, Kinjal Chauhan, Sharad Gupta, Prakash Pillai, Chirayu Pandya, Jyoti V. Thaikoottathil and Sarita S. Gupta. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.