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作 者:高红艳[1] 牛春燕[1] 刘凯歌[1] 吴方雄 汪文[1] 张琦[1]
出 处:《陕西医学杂志》2009年第11期1467-1469,1472,共4页Shaanxi Medical Journal
摘 要:目的:探讨丹参酮ⅡA对大鼠应激性胃粘膜损伤的保护作用。方法:用水浸束缚应激法(WRS)复制大鼠应激性胃粘膜损伤模型,提前7d灌胃给予丹参酮ⅡA,应激6h后处死大鼠,观察胃粘膜损伤指数和胃粘膜损伤程度的变化,检测血清及胃粘膜组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量的变化。结果:大鼠水浸束缚应激后胃粘膜SOD活性明显下降,MDA含量明显升高,可能与应激后氧自由基生成增多有关,从而产生胃粘膜损伤,出现应激性溃疡;丹参酮A能明显降低应激大鼠胃粘膜损伤指数和胃粘膜MDA水平,升高血清和胃粘膜SOD活性。结论:丹参酮ⅡA对水浸束缚应激引起的大鼠胃粘膜损伤有明显的保护作用,可能与其抑制脂质过氧化作用有关。Objective:To evaluate the protective effectsof Tanshinone- Ⅱ A (TanⅡ A) on gastric ulcer in rats induced stress by. Methods: water immersion and restraint stress (WRS) induced gastric injury was used as the experimental model of acute gastric ulcer. Rats were orally administratred with Tan ⅡA before stresse. 6 hours after WRS, all animals were sacrificed and the stomachs of rats were taken out to examine the ulcer index and observe histologically. The activity of total superoxide dismutase (SOD) and malondialdehyde (MDA) were measured in serum and gastric mucosa. Results: 6 hours of water immersion and restraint stress (WRS) resulted in appearance of acute gastric mucosal lesions. Tan Ⅱ A significantly decreased the ulcer index and the activity of SOD both in serum and gastric mucosa. Conclusion: Tan ⅡA has remarkable protective effects on WRS induced gastric ulcer on rats, which is related to inhibiting lipid peroxidation.
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