首页> 中文期刊> 《胃肠病学和肝病学杂志》 >IL-4、IL-13在慢性综合应激模型大鼠Cajal细胞损伤中的作用

IL-4、IL-13在慢性综合应激模型大鼠Cajal细胞损伤中的作用

         

摘要

目的 观察慢性综合应激模型大鼠中IL-4及IL-13的表达变化,并初步探讨其在Cajal细胞(Interstitial cells of Cajal,ICC)损伤中的作用.方法 健康成年SD雄性大鼠20只,随机分为实验组和对照组,每组10只,实验组大鼠制备慢性综合应激模型,旷场实验鉴定造模成功后,采用ELISA法测定血清IL-4、IL-13的浓度,免疫荧光法观察肠道肌间神经丛TMEM16A的表达与分布.结果 模型组和对照组大鼠血清IL-4浓度分别为(8.09±0.97) pg/mL和(6.98±0.69) pg/mL,差异有统计学意义(t=3.363,P<0.01),血清IL-13浓度分别为(5.96±0.67) pg/mL和(5.26±0.73) pg/mL,差异有统计学意义(t=2.322,P<0.05);荧光显微镜下观察肠道平滑肌间神经丛TMEM16A有阳性表达,模型组在不同节段肠道肌间神经丛为阳性表达的细胞减少且分布稀疏.结论 慢性综合应激时,IL-4、IL-13等Th2免疫应答相关炎性因子产生增加,其可能通过调控TMEM16A表达参与了 ICC的损伤.%Objective To observe the expression of IL-4 and IL-13 in rats treated with chronic and comprehensive stress and explore their roles in the damage of interstitial cells of Cajal. Methods Twenty male SD rats were randomly divided into 2 groups; the model group ( n = 10) and the control group ( n = 10). Rats in model group were treated with chronic and comprehensive stress. Open-field test was used to confirm the accomplishment of model. The serum concentration of IL-4 and IL-13 were determined by ELISA and the expression of TMEM16A in the myenterie plexus was detected by immunofluorescence. Results The mean serum concentration of IL-4 in the model group (8. 09 pg/mL +0. 92 pg/mL) was significantly higher than that in the control group (6.98 pg/mL ±0.69 pg/mL) (t =3. 363, P < 0.01 ), while the mean serum concentration of IL-13 in the model group (5. 96 pg/mL ±0. 67 pg/mL) was also significantly higher than that in the control group (5. 26 pg/mL ± 0. 73 ) pg/mL ( t = 2. 322 , P < 0. 05 ) . Positive expression of TMEM16A in the myenterie plexus was observed under the fluorescence microscope. Compared with the control group, the expression of TMEM16A in the model group were decreased in all sections of the intestine. Conclusion In model rats treated with chronic and comprehensive stress, the expression of Th2-related cytokines (IL-4 and IL-13) were increased, and it might result in the damage of interstitial cells of Cajal by affecting the expression of TMEM16A.

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