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目的:探讨消痈溃得康及其拆方对水-束缚应激引起的大鼠胃黏膜损伤的保护作用及机制。方法:将大鼠随机平均分为正常组、模型组、消痈溃得康组、清热解毒组、和血止血组、托里生肌组。每天早晚两次灌胃,正常组和模型组给予等体积生理盐水,连续5天,末次给药1h后造模。取大鼠血、胃,将胃拍照、分割。结果:水-束缚应激引起大鼠胃及血清中谷胱甘肽(Glutataione,GSH)含量降低、脂质过氧化物(Lipid Hydroperoxide,LPO)含量升高,谷胱甘肽过氧化物酶(Glutathione Peroxidase,GPX)、诱导型一氧化氮合酶(Inducible Nitric Oxide Synthase,i NOS)酶活力降低。消痈溃得康及各拆方均能够抑制水-束缚应激引起的大鼠胃黏膜损伤,提高水-束缚应激引起的大鼠胃组织及血清中GSH含量及GPX、i NOS酶活力;降低LPO含量。结论:消痈溃得康及其拆方对水-束缚应激引起的大鼠胃黏膜损伤起到保护,其中托里生肌组药物作用最明显,抗氧化作用可能是其重要的机制之一。
Objective: To investigate the protective effect and mechanism of Xiao-De-De-Kang and its disassembled formulas on gastric mucosal injury induced by water-restraint stress in rats. Methods: The rats were randomly divided into normal group, model group, Xiaokuodekang group, Qingrejiedu group, Hemostatic group and Tory Sang muscle group. Oral administration was given twice a day morning and evening. The normal group and model group were given equal volume of normal saline for 5 consecutive days. The model was established after the last administration for 1 hour. Take the rat blood, stomach, stomach photos, segmentation. Results: The water-restraint stress caused the decrease of Glutataione (GSH) and the content of Lipid Hydroperoxide (LPO) in stomach and serum of rats, the increase of glutathione peroxidase (Glutathione Peroxidase (GPX) and iNOS activity decreased. Elimination of ulcerative Kang and all demolition prescriptions can inhibit water-restraint stress-induced gastric mucosal injury and increase water-restraint stress-induced rat gastric tissue and serum GSH content and GPX, i NOS enzyme activity; Lower LPO content. CONCLUSION: Xiaotong Kang and its disassembled prescriptions protect gastric mucosal injury induced by water-restraint stress in rats, among which the most obvious effect is the drug of Tory Sang muscle group and the anti-oxidative effect may be one of its important mechanisms .