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[目的]观察垂盆草干预三硝基苯磺酸(TNBS)诱导的结肠炎模型大鼠转化生长因子β1(TGF-β1)、白细胞介素2(IL-2)、IL-10的改变,探讨垂盆草是否对结肠炎具有保护作用及其可能作用机制。[方法]30只SD大鼠随机分为3组;模型组及干预组经肛灌入TNBS/乙醇,对照组灌入0.85%氯化钠。造模后干预组给予垂盆草灌胃,对照组及模型组给予0.85%氯化钠,检测炎症活动指数(DAI)、大体形态损伤指数(CMDI)、组织学损伤指数(TDI)的改变,免疫组化检测结肠TGF-β1的表达,ElISA法检测血清IL-2、IL-10。[结果]干预组结肠TGF-β1表达平均光密度(0.21±0.02)较模型组(0.19±0.01)升高;干预组血清IL-10浓度(34.00±6.56)pg/ml较模型组(27.61±4.28)pg/ml升高;干预组血清IL-2浓度(66.70±3.51)pg/ml较模型组(66.70±3.51)pg/ml降低(均P<0.05)。干预组大鼠的DAI、CMDI及TDI与模型组比较差异有统计学意义(均P<0.05)。[结论]垂盆草对TN-BS诱导的实验性结肠炎具有保护作用,可能通过调控T细胞分泌TGF-β1、IL-2、IL-10等细胞因子发挥作用。
[Objective] To observe the changes of transforming growth factor-β1 (TGF-β1), interleukin-2 (IL-2) and interleukin-10 in the rat model of colitis induced by trinitrobenzene sulfonic acid (TNBS). To explore whether Sarbutyra has a protective effect on colitis and its possible mechanism. [Methods] Thirty SD rats were randomly divided into three groups: the model group and the intervention group were anesthetized with TNBS/ethanol, and the control group was infused with 0.85% sodium chloride. After intervention, the intervention group was given intragastric gavage. The control group and the model group were given 0.85% sodium chloride. The changes of DAI, CMDI, and TDI were detected. Immunohistochemistry was used to detect the expression of TGF-β1 in the colon, and serum IL-2 and IL-10 were detected by ElISA. [Results] The average optical density of colon TGF-β1 expression in the intervention group was (0.21±0.02) higher than that in the model group (0.19±0.01); the serum IL-10 concentration in the intervention group was (34.00±6.56) pg/ml compared with the model group (27.61±) 4.28) pg/ml increased; serum IL-2 concentration (66.70±3.51) pg/ml was lower in the intervention group than in the model group (66.70±3.51) pg/ml (all P<0.05). The DAI, CMDI and TDI in the intervention group were significantly different from those in the model group (all P<0.05). [Conclusion] S. sargentii has a protective effect on experimental colitis induced by TN-BS, which may play a role by regulating the secretion of TGF-β1, IL-2, IL-10 and other cytokines by T cells.