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目的:观察小檗碱(Ber)和育亨宾(Y)对LPS诱导的小鼠肠道损伤和肠上皮细胞增殖抑制的影响。方法:雄性BALB/c小鼠随机分为对照组(control)、脂多糖组(LPS)、小檗碱组(Ber+LPS)、小檗碱与育亨宾合剂组(Ber+Y+LPS)、育亨宾组(Y+LPS)、小檗碱组(Ber)、小檗碱和育亨宾合剂组(Ber+Y)及育亨宾组(Y)。分别予以双蒸水、Ber(50mg/kg)、Ber(50mg/kg)+Y(2mg/kg)、Y(2mg/kg)灌胃,1time/d,连续3d,于实验第3d灌胃后1h,腹腔注射生理盐水或LPS(18mg/kg,0.2mL/10g)。观察各组小鼠肠组织形态学、肠黏膜重量和绒毛高度的改变;酶联免疫吸附实验(ELISA)测定肠组织二胺氧化酶(DAO)含量;免疫组化染色方法分析各组肠组织增殖细胞核抗原(PCNA)的表达。结果:LPS组小鼠肠腔显示炎性渗出、出血;肠损伤评分明显高于对照组;LPS组肠黏膜重量、肠绒毛高度、肠组织DAO含量、肠上皮细胞PCNA表达明显低于对照组。与LPS组比较,Ber组、Ber+Y组上述改变明显减轻,但两组间未见明显差异;育亨宾对LPS引起的上述指标变化无明显抑制作用。结论:Ber通过非α2肾上腺素能受体依赖的途径减轻LPS引起的肠上皮细胞增殖抑制和肠道损伤。
Objective: To observe the effects of berberine and yohimbine (Y) on intestinal injury and intestinal epithelial cell proliferation induced by LPS in mice. Methods: Male BALB / c mice were randomly divided into control group, lipopolysaccharide group (LPS), berberine group (Ber + LPS), berberine and yohimbine mixture (Ber + Y + LPS) Y + LPS, Ber, Ber + Y, and Yohimbin. The mice were treated with double distilled water (Ber, 50mg / kg), Ber (50mg / kg) and Y (2mg / kg) 1h, intraperitoneal injection of saline or LPS (18mg / kg, 0.2mL / 10g). The changes of intestinal mucosal morphology, intestinal mucosa weight and villus height were observed in each group. The content of diamine oxidase (DAO) in intestinal tissue was determined by enzyme linked immunosorbent assay (ELISA). The proliferation of intestinal mucosa Nuclear antigen (PCNA) expression. Results: The intestinal mucosa of LPS group showed inflammatory exudation and hemorrhage. The score of intestinal injury was significantly higher than that of control group. The intestinal mucosa weight, intestinal villus height, intestinal DAO content and the expression of PCNA in LPS group were significantly lower than those in control group . Compared with LPS group, the changes in Ber and Ber + Y groups were significantly reduced, but there was no significant difference between the two groups; Yohimbin had no significant inhibitory effect on the above indexes induced by LPS. CONCLUSIONS: Ber attenuates LPS-induced inhibition of intestinal epithelial cell proliferation and intestinal damage through a non-alpha2 adrenergic receptor-dependent pathway.