竹叶黄酮对乙醇诱导小鼠急性胃黏膜损伤的保护作用

Protection of bamboo leaf flavonoids on ethanol-induced acute gastric mucosal injury in mice

目的观察竹叶黄酮对乙醇诱导小鼠急性胃黏膜损伤的保护作用。方法取40只小鼠随机均分为对照组、模型组、维生素E(50 mg/kg)组以及竹叶黄酮25、50 mg/kg组。各组连续ig给药7 d,1次/d。末次给药1 h后,各组按10 mg/kg ig给予无水乙醇,制作胃黏膜损伤模型。建模4 h后,观察胃黏膜损伤面积,计算胃黏膜损伤指数和损伤抑制率。测定小鼠胃黏膜组织中一氧化氮(NO)、前列腺素(PEG2)含量以及血清中超氧化物歧化酶(SOD)、丙二醛(MDA)水平。结果与模型组比较,竹叶黄酮25 mg/kg组小鼠胃黏膜损伤面积减少,50 mg/kg组小鼠损伤程度最小。与模型组比较,竹叶黄酮25、50 mg/kg组小鼠胃黏膜损伤指数均明显降低(P<0.01);胃黏膜组织NO、PEG_2含量明显升高(P<0.01);血清SOD、MDA水平明显降低(P<0.01),SOD/MDA比值明显升高(P<0.01)。结论竹叶黄酮能拮抗乙醇诱导的胃黏膜损伤,其机制可能与其抗氧化、抑制氧自由基产生并升高胃黏膜NO、PEG_2含量有关。

Objective To observe protective effect of bamboo leaf flavonoids on ethanol-induced acute gastric mucosal injury in mice. Methods A total of 40 mice were randomly divided into control group, model group, vitamin E group（50 mg/kg） and bamboo leaf flavonoids 25, 50 mg/kg groups. All the animals were ig administered with drugs for 7 d, once daily. Mice in treatment groups were ig administered with ethanol 10 mL/kg to make acute gastric mucosal injury models 1 h after the last medication. After 4 h model were made, gastric mucosal injury areas were observed, and mucosal injury index and injury inhibition rates were calculated. Contents of NO and PEG2 in gastric mucosa tissue were detected, and in the same times, levels of MDA and the activity of SOD in serum were determined. Results Compared with model group, gastric mucosal injury areas in mice of bamboo leaf flavonoids 25 mg/kg group reduced, and those of bamboo leaf flavonoids 50 mg/kg group were minimum. Compared with model group, gastric mucosal injury index of mice in bamboo leaf flavonoids 25, 50 mg/kg group significantly reduced（P〈0.01）, contents of NO and PEG2 in gastric mucosa tissue obviously increased（P〈0.01）, levels of MDA and SOD in serum were significantly decreased（P〈0.01）, while the value of SOD/MDA significantly increased（P〈0.01）. Conclusion Bamboo leaf flavonoids can prevent ethanol-induced gastric mucosal injury, which perhaps be related to antioxidation, scavenging oxygen free radicals, and increasing the levels of NO and PEG2 in gastric mucosa tissues.