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目的初步研究芸香甙（Ｒｕ）对应激性胃粘膜损伤保护作用的机制。方法采用大鼠冷冻－束缚应激模型，评价胃粘膜损伤指数的变化。ＭＤＡ和ＧＳＨ含量测定分别应用ＴＢＡ和ＤＴＮＢ法，胃粘膜局部血流量（ＧＭＢＦ）测定应用氢气清除法。结果给予Ｒｕ抗溃疡剂量（５，２０ｍｇｋｇ－１，ｉｇ）ｂｉｄ，连续５ｄ，使血清和胃粘膜中因应激而升高的ＭＤＡ含量明显降低，并可升高应激后降低的胃粘膜ＧＳＨ含量。高Ｃａ２＋／低Ｃａ２＋分别可拮抗／增强Ｒｕ的胃粘膜保护作用。Ｒｕ尚可提高应激后降低的ＧＭＢＦ。Ｒｕ的构效关系研究显示，３个剂量（８．２，１６．４，３２．８μｍｏｌｋｇ－１）的Ｒｕ和槲皮素（ｑｕｅｒｃｅｔｉｎ，Ｑｕｅ）均可减轻应激所致的胃粘膜损伤，但Ｒｕ和Ｑｕｅ相同剂量组之间的胃粘膜损伤指数差异无显著性。结论Ｒｕ对应激性胃粘膜损伤保护作用的机制可能与其抗氧化作用、Ｃａ２＋拮抗和改善ＧＭＢＦ有关。Ｒｕ结构中的甙元部分在保护胃粘膜中起主要作用。
Objective To study the mechanism of protective effect of rutin (Ru) on stress-induced gastric mucosal injury. Methods Rat freezing-restraint stress model was used to evaluate the changes of gastric mucosal injury index. The contents of MDA and GSH were determined by TBA and DTNB methods respectively, and the gastric mucosal blood flow (GMBF) was measured by hydrogen gas removal method. Results Ru was given as an antiulcer dose (5,20 mg kg-1, ig) bid for 5 days continuously. The MDA content in serum and gastric mucosa increased significantly due to stress, and the GSH content in gastric mucosa decreased after stress was increased. . High Ca2+/low Ca2+ can antagonize/enhance the protective effect of Ru on gastric mucosa. Ru still can increase the reduced GMBF after stress. Studies on the structure-activity relationship of Ru showed that three doses (8.2, 16.4, 32.8 μmol kg-1) of Ru and quercetin (Que) all relieved gastric mucosal damage caused by stress, but There was no significant difference in the index of gastric mucosal injury between the same dose groups of Ru and Que. Conclusion The protective mechanism of Ru on stress-induced gastric mucosal injury may be related to its antioxidation, Ca2+ antagonism and improvement of GMBF. The part of the Ru structure plays a major role in protecting the gastric mucosa.