Effects of dietary baicalin supplementation on iron overload-induced mouse liver oxidative injury

Eur J Pharmacol. 2005 Feb 21;509(2-3):195-200. doi: 10.1016/j.ejphar.2004.11.060.

Abstract

Iron overload is one of the most common metal related toxicity. Under this circumstance, excessive iron deposition in liver will lead to further injury such as hepatocellular necrosis, inflammation, fibrosis, and in some cases even to carcinoma. In this paper, the effect of a nature flavonoid, baicalin, on iron overload-induced mouse liver oxidative injury has been studied. It was found that when iron-dextran-induced iron overload, mice were fed baicalin-containing diet (0.25% and 1%) for 50 days, hepatic iron, liver-to-body weight ratio, and hepatic lipid peroxidation were dose-dependently decreased; while catalase activity, total antioxidant status, and serum iron content were dose dependently increased. The protective effect of baicalin on liver of iron overload mouse may due to both the antioxidant and iron chelation activities of baicalin. These data provide preliminary experimental support for baicalin as medicine for iron overload diseases.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Antioxidants / metabolism
  • Body Weight / drug effects
  • Catalase / metabolism
  • Dietary Supplements*
  • Flavonoids / administration & dosage
  • Flavonoids / pharmacology*
  • Iron / blood
  • Iron / metabolism
  • Iron Overload / physiopathology*
  • Lipid Peroxidation / drug effects
  • Liver / drug effects*
  • Liver / metabolism
  • Liver / pathology
  • Male
  • Mice
  • Organ Size / drug effects
  • Random Allocation
  • Thiobarbituric Acid Reactive Substances / metabolism
  • Time Factors

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Antioxidants
  • Flavonoids
  • Thiobarbituric Acid Reactive Substances
  • baicalin
  • Iron
  • Catalase