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RISS 인기검색어
- 검색키워드
- 저자 : Subramanian Kaviarasan (검색결과 3 건)
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Fenugreek seed polyphenols inhibit RBC membrane Na<sup>+</sup>/K<sup>+</sup>-ATPase activity
Anuradha, Carani V.,Kaviarasan, Subramanian,Vijayalakshmi, Kodali Kyung Hee Oriental Medicine Research Center 2003 Oriental pharmacy and experimental medicine Vol.3 No.3
The hypoglycemic and hypolipidaemic effects of fenugreek seeds (Trigonella foenum graecum) are well established. Owing to the wide spread use of the seeds by healthy individuals and by diabetic patients we wanted to test whether the seeds can affect biological systems such as membrane transport function. In the present study fenugreek seed polyphenols were extracted and their effect on erythrocyte membrane-bound sodium-potassium adenosine triphosphatase $(Na^+/K^+-ATPase)$ activity was studied in vitro. Fenugreek seed polyphenols inhibited $Na^+/K^+-ATPase$ in erythrocyte membrane of diabetic and normal subjects. Maximum inhibition was observed at $100\;{\mu}l$ of extract containing 0.75 mM gallic acid equivalents. The uncoupling of membrane ATPases in vitro suggest that polyphenols from fenugreek seeds may possess a positive inotropic effect.
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Carani V Anuradha,Subramanian Kaviarasan 경희대학교 융합한의과학연구소 2007 Oriental Pharmacy and Experimental Medicine Vol.7 No.3
The present study was designed to estimate the protective effect of (-) epigallocatechin gallate (EGCG) on ethanol-induced liver injury in rats. Chronic ethanol administration (6 g/kg/day × 60 days) caused liver damage that was manifested by the elevation of markers of liver dysfunction - aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, bilirubin and γ-glutamyl transferase in plasma and reduction in liver glycogen. The activities of alcohol metabolizing enzymes such as alcohol dehydrogenase and aldehyde dehydrogenase were found to be altered in alcohol-treated group. Ethanol administration resulted in the induction of cytochrome p450 and cytochrome-b5 activities and reduction of cytochrome-c reductase and glutathione-S-transferase, a phase II drug metabolizing enzyme. Further, ethanol reduced the viability of isolated hepatocytes (ex vivo) as assessed by trypan blue exclusion test and induced hepatocyte apoptosis as assessed by propidium iodide staining. Treatment of alcoholic rats with EGCG restored the levels of markers of liver injury and mitigated the alterations in alcohol metabolizing and drug metabolizing enzymes and cyt-c-reductase. Increased hepatocyte viability and reduced apoptotic nuclei were observed in alcohol + EGCG-treated rats. These findings suggest that EGCG acts as a hepatoprotective agent against alcoholic liver injury.
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Anuradha, Carani V,Kaviarasan, Subramanian Kyung Hee Oriental Medicine Research Center 2007 Oriental pharmacy and experimental medicine Vol.7 No.3
The present study was designed to estimate the protective effect of (-) epigallocatechin gallate (EGCG) on ethanol-induced liver injury in rats. Chronic ethanol administration (6 g/kg/day ${\times}$ 60 days) caused liver damage that was manifested by the elevation of markers of liver dysfunction - aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, bilirubin and ${\gamma}$-glutamyl transferase in plasma and reduction in liver glycogen. The activities of alcohol metabolizing enzymes such as alcohol dehydrogenase and aldehyde dehydrogenase were found to be altered in alcohol-treated group. Ethanol administration resulted in the induction of cytochrome p450 and cytochrome-$b_{5}$ activities and reduction of cytochrome-c reductase and glutathione-S-transferase, a phase II drug metabolizing enzyme. Further, ethanol reduced the viability of isolated hepatocytes (ex vivo) as assessed by trypan blue exclusion test and induced hepatocyte apoptosis as assessed by propidium iodide staining. Treatment of alcoholic rats with EGCG restored the levels of markers of liver injury and mitigated the alterations in alcohol metabolizing and drug metabolizing enzymes and cyt-c-reductase. Increased hepatocyte viability and reduced apoptotic nuclei were observed in alcohol + EGCG-treated rats. These findings suggest that EGCG acts as a hepatoprotective agent against alcoholic liver injury.
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