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目的:探讨黄芩苷对内毒素-脂多糖(LPS)引起的肠损伤的肠黏膜保护作用及黄芩苷对脓毒血症小鼠回、结肠黏膜抗氧化损伤的保护作用。方法:健康雄性BALB/c小鼠50只随机分为5组:正常对照组、模型组、黄芩苷高、中、低剂量组。分别灌胃双蒸水、黄芩苷100,50,25 mg·kg-1,每日1次,连续3 d,于第3天灌胃后1 h,腹腔注射生理盐水或LPS(17 mg·kg-1),于腹腔注射LPS后20 h处死小鼠,取回、结肠组织。观察各组小鼠生活、精神状态,记录各组小鼠死亡率,取材后测量结肠长度;光镜下根据Chiu肠黏膜损伤评分方法对肠组织进行分级,以HE染色方法观察肠组织病理学变化;采用紫外分光光度法检测肠组织匀浆液总抗氧化能力(T-AOC)、超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-PX);免疫组化染色方法分析各组肠组织PCNA的表达。结果:小鼠腹腔注射LPS后,出现死亡现象,黄芩苷给药组死亡百分率明显低于模型组。黄芩苷中剂量组小鼠结肠长度较模型组显著增加(P<0.05);肠黏膜损伤程度较模型组显著降低,回、结肠的高剂量组损伤较模型组显著降低(P<0.05),回、结肠的中、低剂量组损伤较模型组显著降低(P<0.000 1);中剂量回肠匀浆液T-AOC,T-SOD,GSH-PX较模型组显著增加(P<0.05);黄芩苷组较模型组PCNA表达无显著性差异。结论:黄芩苷有保护肠上皮细胞免受氧自由基损伤的能力,其通过改善肠黏膜结构与功能减轻LPS引起的肠道损伤。
Objective: To investigate the protective effect of baicalin on intestinal mucosa induced by endotoxin-lipopolysaccharide (LPS) -induced intestinal injury and the protective effect of baicalin on the anti-oxidative damage of colonic mucosa in septic mice. Methods: Fifty healthy male BALB / c mice were randomly divided into 5 groups: normal control group, model group and baicalin high, medium and low dose groups. Double distilled water, baicalin 100,50,25 mg · kg-1, once daily for 3 consecutive days, were intraperitoneal injected with normal saline or LPS (17 mg · kg -1 -1). The mice were killed 20 h after LPS injection, and the colon tissues were removed. The life and mental status of mice in each group were observed, and the mortality of mice in each group was recorded. The length of colon was measured after taking the materials. The intestinal tissue was graded by Chiu intestinal mucosal injury score under light microscope. The pathological changes of intestinal tissue were observed by HE staining. The total antioxidant capacity (T-AOC), superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-PX) in intestinal homogenate were detected by UV spectrophotometry. Methods The expression of PCNA in each group was analyzed. Results: The mice died after intraperitoneal injection of LPS. The percentage of death in baicalin administration group was significantly lower than that in model group. Compared with the model group, the length of colon of baicalin middle dose group was significantly increased (P <0.05), and the damage of intestinal mucosa was significantly lower than that of the model group (P <0.05) (P <0.0001). The levels of T-AOC, T-SOD and GSH-PX in the medium dose ileum homogenate were significantly increased compared with the model group (P <0.05) There was no significant difference in PCNA expression between the model group and the model group. CONCLUSION: Baicalin has the ability to protect intestinal epithelial cells from damage by oxygen free radicals, which can reduce intestinal damage caused by LPS by improving intestinal mucosa structure and function.