USE OF FICUS VIRENS AIT EXTRACT AND NOVEL COMPOUND ISOLATED THEREFOM AGAINST -HYDROXY--METHYLGLUTARYL-COA REDUCTASE INHIBITORY ACTIVITY, HYPERLIPIDEMIA AND OXIDATIVE STRESS.
MOHAMMAD SALMAN KHAN,DANISH IQBAL,MD SARFRAJ HUSSAIN
申请号：
IN308/DEL/2014
公开号：
IN2014DE00308A
申请日:
2014.02.03
申请国别(地区):
IN
年份:
2014
代理人:
摘要：
The present study was done to evaluate the most potent antioxidant and -hydroxy-Pmethylglutaryl-CoA reductase (HMGR) inhibitor from sequentially extracted fraction of Ficus virens Ait., as well as to isolate and purify the bioactive compound responsible for these activity. Our results shows that of all the sequentially extracted fraction of F. virens bark and leaves extract, F. virens bark methanol extract exhibits strong radical scavenging and antioxidant activity. In addition, F. virens bark methanol extract, which is non- cytotoxic, significantly and most potently inhibit the HMGR activity (IC50=3.45+-0.45 ug/ml) in comparison to other extracts. Further, the most potent bioactive fraction F18 was isolated from Ficus virens bark methanolic extract as a reddish brown crystal and subjected to IR, 1H NMR, 13C NMR and mass spectroscopy analysis to identify this compound. Our data showed it as a novel compound, n- Octadecanyl-0- a-D-glucopyranosyl (6+1) -0- a-D-glucopyranoside with a molecular weight of 594, that exhibits significant HMGR inhibitory activity in vitro (98.5%) at 5pg/ml and demonstrated uncompetitive mode of inhibition against HMGCoA reductase. Moreover, the in vivo hypolipidemic activity of FVBM extract and compound isolated therefrom were also evaluated against Tyloxapol induced hyperlipidemia in rats. The inventor for the first time reported a significant reduction in TC, TG and LDL-C with a increase in HDL-C level in FVBM extract (500 mglkg & 1000 mgkg) and pure bioactive compound (10mgkg) treated rats when compared to Tyloxapol induced hyperlipidemic control rats. These findings suggest that the extract or the bioactive compound isolated therefrom could be used in the treatment of risk factor induced hperlipidemia.
