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目的:研究罗汉果皂苷总提物(ME,mogrosides extract)对大鼠小肠微血管动脉在高血糖环境下内皮完整血管的舒张保护作用,并探讨其作用机制。方法:置微血管动脉于22.5 mmol/L的高糖缓冲液中预孵育1 h,采用10 mmol/L甲氧氨(methoxamine)预收缩血管,观察ME在给药后于高糖环境下血管舒张功能;另外分别使用了吲哚美辛、NO抑制剂L-NAME及树突毒素+蜂毒明肽,通过观察不同抑制剂在高糖加药组中对微血管舒张的影响,研究ME对血管收缩舒张的相关因素。结果:与空白对照组(葡萄糖:5.5 mmol/L)相比,高糖模型组血管的舒张能力明显减弱,而高糖加药组(葡萄糖:22.5mmol/L+100μg/ml,ME)对比高糖模型组(葡萄糖:22.5mmol/L)则显着地增强了血管的舒张能力;引哚美辛及L-NAME及树突毒素+蜂毒明肽的加入均对高糖加药组的结果有所改变。结论:ME于高糖的环境下可增加血管的舒张作用,主要的保护作用来源于增强了血管自身的舒张因子的功能,特别是促进了环氧合酶及NO生成这两条路径。
Objective: To study the protective effect of mogrosides extract on the vasodilatation of endothelium-intact vessels in the small intestine microvascular in rats under hyperglycemia and to explore its mechanism. Methods: The microvascular arteries were pre-incubated for 1 h in 22.5 mmol / L high glucose buffer. The vessels were pre-contracted with 10 mmol / L methoxamine to observe the effects of ME on the vasodilatation In addition, indometacin, NO inhibitor L-NAME and dendritetoxin + bee venom peptide were respectively used to study the effects of different inhibitors on vasodilatation in hyperglycemic drug-addition group. Related factors. RESULTS: Compared with the blank control group (glucose: 5.5 mmol / L), the vasodilatation in high glucose group was significantly decreased, while the high glucose group (glucose: 22.5mmol / L + 100μg / ml, ME) Glycose model group (glucose: 22.5mmol / L) significantly increased the vasodilatation; indomethacin and L-NAME and dendritic toxin + bee venom peptide were added on the results of high glucose group Changed. CONCLUSION: ME can increase the vasodilation of blood vessels in high glucose environment. The main protective effect is due to the enhancement of the vasodilator’s own relaxation factor, especially the promotion of the two pathways of cyclooxygenase and NO production.