目的 觀察竹葉黃酮對乙醇誘導(dǎo)小鼠急性胃黏膜損傷的保護(hù)作用.方法 取40 只小鼠隨機(jī)均分為對照組、模型組、維生素E(50 mg/kg)組以及竹葉黃酮25、50 mg/kg 組.各組連續(xù)ig 給藥7 d,1 次/d.末次給藥1 h 后,各組按10 mg/kg ig給予無水乙醇,制作胃黏膜損傷模型.建模4 h 后,觀察胃黏膜損傷面積,計(jì)算胃黏膜損傷指數(shù)和損傷抑制率.測定小鼠胃黏膜組織中一氧化氮(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.結(jié)果 與模型組比較,竹葉黃酮25 mg/kg 組小鼠胃黏膜損傷面積減少,50 mg/kg 組小鼠損傷程度最小.與模型組比較,竹葉黃酮25、50 mg/kg 組小鼠胃黏膜損傷指數(shù)均明顯降低(P< 0.01);胃黏膜組織NO、PEG₂ 含量明顯升高(P< 0.01);血清SOD、MDA水平明顯降低(P< 0.01),SOD/MDA 比值明顯升高(P< 0.01).結(jié)論 竹葉黃酮能拮抗乙醇誘導(dǎo)的胃黏膜損傷,其機(jī)制可能與其抗氧化、抑制氧自由基產(chǎn)生并升高胃黏膜NO、PEG₂ 含量有關(guān).

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.