Endothelium-dependent and-independent relaxation induced by curcumin in rat superior mesenteric arte

来源 :第十五届中国西部实验动物管理与学术交流会 | 被引量 : 0次 | 上传用户:wanganInsh888
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  Curcumin (Cur), a natural lipophilic polyphenol compound extracted from the rhizome of turmeric (Curcuma longa).Recently, protective effect of Cur on cardiovascular system is pay close attention.Some researches demonstrated that Cur could induce vascular relaxation in many arterial beds.However, relaxant effect of Cur on rat superior mesenteric artery, and its mechanism are not clear.The aim of present study was to investigate the vasorelaxant effect of Cur on rat superior mesenteric arteries and the mechanisms involved.The isometric tension of rat superior mesenteric arterial rings was recorded in vitro on a myograph.Cur concentration-dependently relaxed the superior mesenteric artery rings with endothelium pre-contracted by PE (Emax=84.33 ± 1.11%;pD2=5.03 ± 0.02) or KCl (Emax=80.96 ± 2.12%;pD2=4.32 ± 0.01).The vasorelaxant effect of Cur on the superior mesenteric artery rings relied on endothelium partially.indomethacin (5 μ M) significantly inhibited the effect.Hovever, 1 H-[1,2,4]Oxadiazolo [4,3-a]quinoxalin-1-one (10 μM) and N ω-nitro-L-arginine methyl ester (L-NAME, 100 μM) had no effect on the action.In artery rings without endothelium, vasorelaxation induced by Cur was attenuated by 4-aminopyridine (100 μ M).However,barium chloride dehydrate (10 μ M), glibenclamide (10 μ M) and traethylammonium chloride (1 mM) did not affect vasorelaxation induced by simvastatin.Moreover, Cur also significantly inhibited contraction induced by increasing external calcium in Ca2+-free medium plus K+ (60 mM) and releasing intracellular Ca2+ in the Ca2+-free solution.Our results suggested that Cur induces relaxation in superior mesenteric arterial rings through an endothelium-dependent pathway, involving prostanoid production, and also through an endothelium-independent pathway, opening voltage-dependent K+ channel, and blockade of extracellular Ca2+ influx and intracellular Ca2+ release.
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