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目的:研究大黄素对小鼠肠缺血再灌注肠黏膜肥大细胞活性的影响。方法:28只昆明种小鼠随机均分为4组,假手术组(A组)、模型组(B组)、模型+大黄素60 mg.kg-1组(D1组)及模型+大黄素120 mg.kg-1组(D2组)。采用肠系膜上动脉夹闭法建立小肠缺血再灌注模型,观察肠黏膜病理结构变化、肠黏膜肥大细胞超微结构变化及类胰蛋白酶表达、比较计算肥大细胞数量,测定小肠组织组胺、肿瘤坏死因子-α(TNF-α)浓度。结果:与假手术组比较,模型组Chiu’s评分、肥大细胞数量、组胺及TNF-α浓度显著增加(P<0.05或P<0.01)。与模型组比较,大黄素60,120 mg.kg-1组的肥大细胞数量明显减少(P<0.05),大黄素120 mg.kg-1组的小肠组织TNF-α浓度明显降低(P<0.05)。假手术组肥大细胞超微结构正常,模型组肥大细胞颗粒包膜相互融合形成细胞内空泡等脱颗粒现象,大黄素60,120 mg.kg-1组肥大细胞形成空泡较少。结论:大黄素能减少小鼠小肠黏膜结构破坏,抑制小肠肥大细胞活化及脱颗粒,从而起到防治肠缺血再灌注损伤的作用。
Objective: To study the effect of emodin on intestinal mucosal mast cell activity in mice with intestinal ischemia reperfusion. Methods: Totally 28 Kunming mice were randomly divided into 4 groups: sham operation group (A group), model group (B group), model + emodin 60 mg.kg-1 group (D1 group) and model + emodin 120 mg.kg-1 group (D2 group). The intestinal ischemia-reperfusion model was established by the superior mesenteric artery occlusion. The pathological changes of the intestinal mucosa were observed. The ultrastructural changes of intestinal mucosa and the expression of tryptase were observed. The number of mast cells, histamine and tumor necrosis Factor-α (TNF-α) concentrations. Results: Compared with the sham operation group, the Chiu’s score, the number of mast cells, the concentration of histamine and TNF-α in model group were significantly increased (P <0.05 or P <0.01). Compared with the model group, the number of mast cells in emodin 60,120 mg.kg-1 group was significantly decreased (P <0.05), and the concentration of TNF-α in intestinal tissue of emodin 120 mg.kg-1 group was significantly decreased (P <0.05). The ultrastructure of mast cells in sham-operated group was normal. The mast cells in the model group were fused with each other to form intracellular vacuoles and other degranulation. Emodin 60 and 120 mg.kg-1 groups formed less vacuoles in mast cells. Conclusion: Emodin can reduce intestinal mucosal damage in mice, inhibit the activation and degranulation of intestinal mast cells, and thus play a role in prevention and treatment of intestinal ischemia-reperfusion injury.