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Lupeol protects against acetaminophen-induced oxidative stress and cell death in rat primary hepatocytes

Food Chem Toxicol. 2012 May;50(5):1781-9. doi: 10.1016/j.fct.2012.02.042. Epub 2012 Mar 3.

Abstract

Drug induced hepatotoxicity is a major problem where phytochemicals hold promise for its abrogation. This study was carried out to explore cytoprotective potential of lupeol, a triterpene, against acetaminophen (AAP)-induced toxicity in rat hepatocytes. AAP exposure significantly (p<0.05) reduced cell viability, disturbed Bcl-2 family pro/anti-apoptotic protein balance, increased ROS production and altered redox homeostasis. It also induced mitochondria-mediated hepatocellular injury by significant mitochondrial depolarization, caspase-9/3 activation and subsequent DNA fragmentation. Our results suggest that lupeol pre-treatment effectively restored antioxidant enzyme levels, decreased lipid peroxidation, inhibited ROS generation and depolarization of mitochondria. Lupeol also attenuated mitochondria-mediated signaling pathway and DNA damage as evident from TUNEL assay and cell cycle studies leading to prevention of cytotoxicity. This study confirms the efficacy of lupeol, a food derived antioxidant, in abrogating ROS generation, maintaining redox balance and providing significant protection against mitochondria-mediated cell death during AAP-induced toxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetaminophen / antagonists & inhibitors*
  • Acetaminophen / toxicity
  • Animals
  • Apoptosis / drug effects*
  • Blotting, Western
  • Flow Cytometry
  • Hepatocytes / drug effects*
  • Hepatocytes / enzymology
  • Hepatocytes / metabolism
  • In Situ Nick-End Labeling
  • Lipid Peroxidation / drug effects
  • Male
  • Oxidative Stress / drug effects*
  • Pentacyclic Triterpenes / pharmacology*
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species / metabolism

Substances

  • Pentacyclic Triterpenes
  • Reactive Oxygen Species
  • Acetaminophen
  • lupeol