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Rutin attenuates cisplatin induced renal inflammation and apoptosis by reducing NFκB, TNF-α and caspase-3 expression in wistar rats.

Abstract
Cisplatin is an effective chemotherapeutic agent that displays dose-limiting nephrotoxicity. In the present study the wistar rats were subjected to concurrent prophylactic oral treatment of rutin (75 and 150 mg/kgb.wt.) against the nephrotoxicity induced by intraperitoneal administration of cisplatin (7 mg/kgb.wt.). Efficacy of rutin against the nephrotoxicity was evaluated in terms of biochemical estimation of antioxidant enzyme activities, histopathological changes and expression levels of molecular markers of inflammation and apoptosis. Rutin pretreatment prevented deteriorative effects induced by cisplatin through a protective mechanism that involved reduction of increased oxidative stress as well as caspase-3, TNF-α and NFκB protein expression levels. We found that the beneficial effect of rutin pretreatment is mediated partially by its inhibitory effect on NFκB and TNF-α pathway mediated inflammation, caspase-3 mediated-tubular cell apoptosis, as well as by restoration of histopathological changes against cisplatin administration.
AuthorsWani Arjumand, Amlesh Seth, Sarwat Sultana
JournalFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association (Food Chem Toxicol) Vol. 49 Issue 9 Pg. 2013-21 (Sep 2011) ISSN: 1873-6351 [Electronic] England
PMID21605616 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2011 Elsevier Ltd. All rights reserved.
Chemical References
  • Antineoplastic Agents
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Rutin
  • Caspase 3
  • Cisplatin
Topics
  • Animals
  • Antineoplastic Agents (pharmacology)
  • Apoptosis (drug effects)
  • Caspase 3 (metabolism)
  • Cisplatin (pharmacology)
  • Inflammation (prevention & control)
  • Kidney (drug effects, pathology)
  • Male
  • NF-kappa B (metabolism)
  • Rats
  • Rats, Wistar
  • Rutin (pharmacology)
  • Tumor Necrosis Factor-alpha (metabolism)

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