Synergistic salubrious effect of ferulic acid and ascorbic acid on membrane-bound phosphatases and lysosomal hydrolases during experimental myocardial infarction in rats.
Altered membrane integrity has been suggested as a major factor in the development of cellular injury during myocardial necrosis. The present study was designed to investigate the effect of the combination of ferulic acid (FA) and ascorbic acid (AA) on lysosomal hydrolases and membrane-bound phosphatases during isoproterenol (ISO) induced myocardial necrosis in rats. Induction of rats with 1SO (150 mg/kg b.wt, i.p.) for 2 days resulted in a significant increase in the activities of lysosomal hydrolases (beta-D-glucuronidase, beta-D-galactosidase, beta-D-N-acetylglucosaminidase, acid phosphatase and cathepsin-D) in the heart and serum. A significant increase in plasma lactate level, cardiac levels of sodium, calcium and a decrease in cardiac level of potassium was also observed, which was paralleled by abnormal activities of membrane-bound phosphatases (Na(+)-K(+) ATPase, Ca(2+) ATPase and Mg(2+) ATPase) in the heart of ISO-administered rats. Pre-co-treatment with the combination of FA (20 mg/kg b.wt) and AA (80 mg/kg b.wt) orally for 6 days significantly attenuated these abnormalities and restored the levels to near normalcy when compared to individual drug treated groups. The combination of FA and AA preserved the membrane integrity by mitigating the oxidative stress and associated cellular damage more effectively when compared to individual treatment groups. In our study, the protection conferred by FA and AA might be through the nitric oxide pathway and by their ability of quenching free radicals. In conclusion, these findings indicate the synergistic modulation of lysosomal hydrolases and membrane phosphatases by the combination of FA and AA.
Yogeeta
Surinder Kumar
SK
Department of Biochemistry, University of Madras, Guindy Campus, Chennai-600 025, Tamilnadu, India.
Gnanapragasam
Arunachalam
A
Senthilkumar
Subramanian
S
Subhashini
Rajakannu
R
Devaki
Thiruvengadam
T
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D001205:Ascorbic Acid / Q000819:agonists / Q000494:pharmacology* / Q000627:therapeutic use; D002316:Cardiotonic Agents / Q000633:toxicity; D002462:Cell Membrane / Q000201:enzymology* / Q000473:pathology; D003373:Coumaric Acids / Q000819:agonists / Q000494:pharmacology*; D004357:Drug Synergism; D005609:Free Radicals / Q000378:metabolism; D007545:Isoproterenol / Q000633:toxicity; D008247:Lysosomes / Q000201:enzymology* / Q000473:pathology; D008297:Male; D009203:Myocardial Infarction / Q000139:chemically induced / Q000188:drug therapy / Q000201:enzymology* / Q000473:pathology; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D009336:Necrosis / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D002316:Cardiotonic Agents; D003373:Coumaric Acids; D005609:Free Radicals; D009569:Nitric Oxide; C004999:ferulic acid; D010744:Phosphoric Monoester Hydrolases; D007545:Isoproterenol; D001205:Ascorbic Acid