Premium
Mechanism of protective action of mangiferin on suppression of inflammatory response and lysosomal instability in rat model of myocardial infarction
Author(s) -
Prabhu S.,
Narayan Shoba,
Devi C. S. Shyamala
Publication year - 2009
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2549
Subject(s) - mangiferin , tumor necrosis factor alpha , lysosome , chemistry , medicine , cathepsin b , endocrinology , mechanism of action , pharmacology , necrosis , inflammation , myocardial infarction , enzyme , biochemistry , in vitro
Lysosomal instability has been suggested as a major factor in the development of cellular injury during myocardial necrosis through the formation of inflammatory mediators. The present study was designed to investigate the effect of mangiferin on lysosomal hydrolases and TNF‐ α production during isoproterenol (ISPH) induced myocardial necrosis in rats. The rats given ISPH (200 mg/kg body weight twice, subcutaneous) for 2 days showed a significant increase in plasma TNF‐ α production, serum and heart lysosomal hydrolases activity. ISPH administration to rats resulted in decreased stability of the membranes, which was reflected by the lowered activity of cathepsin‐D and β ‐glucuronidase in mitochondrial, nuclear, lysosomal and microsomal fractions. Pretreatment with mangiferin (100 mg/kg body weight, intraperitoneally) for 28 days, significantly prevented the alterations and restored the enzyme activities to near‐normal status. These findings demonstrate that mangiferin could preserve lysosomal integrity through decrease in the inflammatory process and hence establish the cardioprotective effect of mangiferin. Copyright © 2009 John Wiley & Sons, Ltd.