Program

PO1-3-10

NEPHROPROTECTIVE POTENTIAL OF GREEN TEA EXTRACT IN EXPERIMENTAL INDUCED KIDNEY DYSFUNCTION

[Speaker] S L Harikumar:1
[Co-author] M. Jothi:1, Hardeep Kaur:1, Gurfateh Singh:1
1:UNIVERSITY SCHOOL OF PHARMACEUTICAL SCIENCES, RAYAT BAHRA UNIVERSITY SAHARUAN SAS NAGAR PUNJAB 140104 INDIA

Background: Nephrotoxicity is a leading disorders worldwide & arises as result of exposure to external agents like drugs including environmental chemicals. Therefore the present study has been designed to investigate the possible involvement of mitochondria permeability transition pore (MPTP), a molecular mechanism as a nephroprotective potential of green tea extract.
Methods: Experimental nephrotoxicity induced in wistar rats by injecting intra-peritoneal injection of Gentamicin (80 mg/kg body weight/day) for six consecutive days started from 10th to 15th day of experimental protocol. The administration of GTE (100 & 200 mg/kg body weight/day/p.o) and Atractyloside, a selective MPTP opener, (5mg/kg, p.o.) started from the 1st day to 15th day of experimental protocol. The animals were sacrificed for the estimation of index of injury and oxidative stress of the kidney on 16th days.
Results: The Gentamicin induced nephrotoxicity, which were assessed in term of significant increase in blood urea nitrogen, serum creatinine levels. Moreover, oxidative stress was noticed in renal tissue as evidenced by a significant decrease in glutathione level, superoxide dismutase also a significant increase in TBARS levels. It is noted that severe degeneration of tubular cells, cloudy cell swelling of tubule & glomeruli, damage of brush border line was confirmed by histopathological study of rat kidney. Pre administration of green tea extract 100 & 200 mg/kg once daily for 15 days of experimental protocol restored normal renal functions by reduced oxidative stress, cellular toxicity, inflammation and glomeruli and tubular Gentamicin induced kidney damages in rats. Atractyloside treated for 15 days reported swelling, inflammation, damage of tubule and glomeruli of rat kidney.
Conclusions: However GTE (high dose) significantly restored normal architecture of kidney and ameliorated Gentamicin induced histopathological changes and this protection was founded to be attenuated on treatment with Atractyloside may be due to opening of MPTP in the present study. Hence, the protective effect of GTE was achieved due to its biological potential may be by closing of MPTP which was further confirmed by its attenuation using atractyloside an MPTP opener in the present study.

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