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Schisandra chinensis extract induced the mechanism of vasorelaxation in rat thoracic aorta

Date:2015/12/15 9:40:57

Schisandra chinensis extract (SC)is a known medical herb for the treatment of cardiovascular symptoms associated with menopausal symptoms in Korea. 

However, the pharmacological action mechanisms of Schisandra chinensis extract involved have not been well studied. This study was aimed to investigate the vascular effects of Schisandra chinensis extract  in rat thoracic aorta.

We isolated the hexane, chloroform, and methanol extracts from Schisandra chinensis extract  and evaluated their vasodilatory effects in the rat thoracic aorta.Hexane extracts of Schisandra chinensis extract  (SCHE, 5 x 10(-5) to 10(-3) g/L) caused a concentration-dependent relaxation in both endothelium-intact and -denuded aortas. The relaxant effect of Schisandra chinensis extract  on the endothelium-intact aorta was more prominent than on the endothelium-denuded aorta. The former was significantly attenuated by L-NAME, a nitric oxide synthase inhibitor, and ODQ, a soluble guanyl cyclase inhibitor, but not by tetraethylammonium, a nonselective blocker of K(+) channels, and indomethacin, a cyclooxygenase inhibitor. Furthermore, Schisandra chinensis extract caused nitrite production as well as ENOS activation in aortic segments, suggesting implication of NO signal pathway in SCHE-induced relaxation. 

In endothelium-denuded aorta, SCHE-induced vasorelaxation was also attenuated by calyculin A, an inhibitor of myosin light chain (MLC) phosphatase, but not by ML-9, a MLC kinase inhibitor, suggestive of implication of MLC phosphatase activation. Phenylephrine-enhanced MLC phosphorylation ratio was significantly attenuated by Schisandra chinensis extract , which was recovered to the control level by pretreatment with calyculin a.taken collectively.

These findings suggest that the vascular relaxation evoked by Schisandra chinensis extract was mediated by not only endothelium dependent NO pathway but also direct effect on vascular smooth muscle cell via dephosphorylation of MLC.