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目的观察丹参酮IIA对葡聚糖硫酸钠(DSS)诱导的小鼠实验性结肠炎是否有干预效果以及对结肠黏膜中性粒细胞浸润和活化的影响,旨在探讨丹参酮IIA治疗结肠炎的作用机制。方法随机将30只C57BL/6小鼠分为正常对照组、DSS组和DSS+丹参酮IIA干预组,每组10只动物;其中模型组给予3%DSS溶液喂饲7 d,干预组小鼠在给予3%DSS溶液喂饲的同时给予丹参酮IIA(200 mg/kg)腹腔注射,1次/d;期间对小鼠疾病活动指数(DAI)进行评分。染毒7 d后处死小鼠,取结肠组织进行病理学检查;采用异硫氰酸荧光素标记葡聚糖(FITC-dextran)法检测小鼠肠黏膜通透性;采用免疫荧光染色方法检测结肠组织Ly6G的表达,并检测MPO活性和炎症因子的水平。结果和正常对照组相比,DSS组小鼠第7天时出现体重减轻、便血和腹泻等症状,DAI显著增高。丹参酮IIA干预明显减轻小鼠结肠炎性损伤,表现为干预组小鼠DAI低于DSS组,差异有统计学意义(P<0.05);干预组小鼠结肠组织病理损伤显著减轻,肠黏膜穿透性亦低于DSS组(P=0.032)。此外,和DSS组相比,丹参酮IIA干预组小鼠结肠组织中性粒细胞浸润和活化程度明显减少,并伴有炎症因子水平显著下降(P<0.05)。结论在本实验条件下,丹参酮IIA对小鼠实验性结肠炎有明显的治疗作用,其机制可能与抑制中性粒细胞浸润、活化和减少炎症因子生成有关。
Objective To observe the effect of tanshinone IIA on dextran sodium sulfate (DSS) induced experimental colitis in mice and its effect on the infiltration and activation of colonic mucosal neutrophils in order to explore the mechanism of action of tanshinone IIA in the treatment of colitis . Methods 30 C57BL / 6 mice were randomly divided into normal control group, DSS group and DSS + tanshinone IIA intervention group, with 10 animals in each group. The model group was given 7% DSS solution for 7 days, 3% DSS solution was given while tanshinone IIA (200 mg / kg) intraperitoneal injection, 1 / d; mouse disease activity index (DAI) were scored. The mice were killed after 7 days of exposure and the colon tissues were taken for pathological examination. The intestinal mucosal permeability of mice was detected by FITC-dextran method. The colon was detected by immunofluorescence staining The expression of Ly6G was assayed and the levels of MPO activity and inflammatory cytokines were measured. Results Compared with the normal control group, on the 7th day in the DSS group, the symptoms of weight loss, blood in the stool and diarrhea appeared and DAI was significantly increased. Tanshinone IIA significantly reduced colonic inflammatory injury in mice, showing that the DAI in the intervention group was lower than that in the DSS group (P <0.05); the pathological damage of the colon tissue in the intervention group was significantly reduced, the intestinal mucosa was penetrated Sex was also lower in the DSS group (P = 0.032). In addition, tanshinone IIA-treated mice significantly decreased the number of neutrophil infiltration and activation, accompanied by a significant decrease in inflammatory cytokines (P <0.05). Conclusion Under the experimental conditions, tanshinone IIA has a significant therapeutic effect on experimental colitis in mice. The mechanism may be related to the inhibition of neutrophil infiltration, activation and reduction of inflammatory cytokines.