Endothelium-dependent and direct relaxation induced by ethyl acetate extract from Flos Chrysanthemi in rat thoracic aorta
Endothelium-dependent and direct relaxation induced by ethyl acetate extract from Flos Chrysanthemi in rat thoracic aorta
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DOI：
10.1016/j.jep.2005.04.018
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发表时间：
2005-10-03
影响因子：
5.4
通讯作者：
Xia, Q
中科院分区：
文献类型：
--
作者：
Jiang, HD;Cai, J;Xia, Q
研究菊花乙酸乙酯提取物（FCE）对大鼠胸主动脉的血管活性及其作用机制。FCE （9.4-150 mg/L）可引起苯肾上腺素（PE, 10(-6) M）或高水平K+（6 × 10(-2) M）预收缩的完整内皮环的浓度依赖性松弛。去除内皮细胞后，其作用虽未完全消除，但明显减弱。n - g -硝基- l -精氨酸甲酯（L-NAME） （10(-4) M）、亚甲基蓝（10(-5)M）显著抑制FCE的作用。与对照组相比，FCE组主动脉NO合成酶明显升高。而吲哚美辛对FCE效果无明显影响。SKF-525A与L-NAME联合使用的效果与L-NAME相同。四乙基铵、BaCl2、4-氨基吡啶、5-HD和心得安也不影响FCE的血管作用，但格列苯脲明显减弱其血管舒张作用。FCE不减少PE在Ca2+无介质中引起的短暂性收缩，但抑制PE在K+无溶液中引起的收缩或PE在Ca2+无溶液中引起稳定收缩后Ca2+引起的收缩。结果表明，FCE可诱导内皮依赖性松弛和非依赖性松弛。NO和cgmp介导的途径可能参与了内皮依赖性松弛，而电压依赖性Ca2+通道的抑制、受体操作的Ca2+通道和K-ATP的激活部分参与了内皮依赖性松弛。2005爱思唯尔爱尔兰有限公司版权所有。
The aims of the present study were to investigate the vasoactive effects of ethyl acetate extract from Flos Chrysanthemi (FCE) and its mechanisms on the rat thoracic aorta. FCE (9.4-150 mg/L) caused a concentration-dependent relaxation on endothelium-intact rings precontracted with phenylephrine (PE, 10(-6) M) or a high level of K+(6 x 10(-2) M). By removal of endothelium, the effect was not abolished but reduced significantly. N-G-nitro-L-arginine methyl ester (L-NAME) (10(-4) M), methylene blue (10(-5) M) significantly inhibited the effect of FCE. Meanwhile, NO synthase of aorta in FCE group was markedly elevated versus the control. However, indomethacin did not influence FCE effect. SKF-525A combined with L-NAME had the same effect as L-NAME. Tetraethylammonium, BaCl2, 4-aminopyridine, 5-HD and propranolol also did not influence the vascular effect of FCE, but glibenclamide significantly attenuated its vasodilation. FCE did not reduce PE-induced transient contraction in Ca2+-free medium, but inhibited PE-induced contraction in K+-free solution or Ca2+ caused contraction after PE induced a stable contraction in Ca2+-free solution. It is concluded that FCE induced both endothelium-dependent and -independent relaxation. NO and cGMP-mediated pathway are likely involved in the endothelium-dependent relaxation, whereas inhibition of voltage-dependent Ca2+ channel, receptor-operate Ca2+ channel and activation of K-ATP contribute in part to the endothelium-independent relaxation. (C) 2005 Elsevier Ireland Ltd. All rights reserved.