Planta Med 2007; 73(15): 1537-1542
DOI: 10.1055/s-2007-993757
Pharmacology
Original Paper
© Georg Thieme Verlag KG Stuttgart · New York

Gomisin A from Schisandra chinensis Induces Endothelium-Dependent and Direct Relaxation in Rat Thoracic Aorta

Ji Young Park1 [*] , Seung Jin Lee1 , Mi Ran Yun1 , Kyo Won Seo1 , Sun Sik Bae1 , June Woo Park2 , You Jin Lee3 , Woo Jung Shin3 , Young Whan Choi3 [*] , Chi Dae Kim1
  • 1Department of Pharmacology, College of Medicine, and MRC for Ischemic Tissue Regeneration and Medical Research Institute, Pusan National University, Busan, Korea
  • 2Department of Neurosurgery, Busan Medical Center, Busan, Korea
  • 3College of Natural Resources & Life Sciences, Pusan National University, Gyeongnam, Korea
Further Information

Publication History

Received: May 25, 2007 Revised: October 24, 2007

Accepted: October 30, 2007

Publication Date:
07 December 2007 (online)

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Abstract

Schisandra chinensis (SC), a member of the Magnoliaceae family, has been used to improve the vascular health for postmenopausal women in Korea. In order to provide some scientific rationales for such effectiveness, this study investigated the vascular effects of gomisin A (GA) from SC. In the endothelium (ED)-intact rings of rat thoracic aorta, GA (1 × 10-6 to 3 × 10-4 M) caused a concentration-dependent relaxation which was markedly attenuated not only by removal of ED but also by pretreatment with N G-nitro-L-arginine (10-4 M) or 1H-[1] [2] [4]oxadiazolo[4,3-a]quinoxalin-1-one (3 × 10-5 M). Direct measurement of nitrite, a metabolite of nitric oxide (NO), confirmed that NO production in isolated aorta was increased by GA. In the ED-denuded specimens, the relaxation by GA was not abolished but reduced significantly. The relaxation by GA in ED-denuded aortic rings were clearly inhibited by calyculin A (3 × 10-8 M), an inhibitor of MLC phosphatase. Furthermore, the phenylephrine-enhanced phosphorylation ratio of MLC was significantly attenuated by GA. Based on these results, it is suggested that GA induced vascular relaxation by partially activating ED-dependent NO pathway, and partially dephosphorylation of MLC.