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目的探讨西酞普兰对慢性应激大鼠血糖及免疫系统的影响。方法 32只雄性SD大鼠随机分为对照组、应激组、实验1组和实验2组。采用强迫游泳建立慢性应激模型。测量血糖和肾上腺、胸腺、脾脏指数,免疫组织化学检测胸腺细胞B细胞淋巴瘤/白血病-2(Bcl-2)、Bcl相关蛋白(Bax)表达水平,TUNEL检测胸腺细胞凋亡情况。结果与应激组比较,对照组大鼠在第20天、第29天血糖降低,实验组大鼠在第29天血糖降低(P<0.05);与对照组比较,实验组在第20天血糖增高(P<0.05)。与应激组比较,对照组、实验1组大鼠肾上腺指数下降、胸腺及脾脏指数上升(P<0.05);与对照组比较,实验2组大鼠胸腺、脾脏指数下降(P<0.01);与实验1组比较,实验2组大鼠胸腺、脾脏指数下降(P<0.05)。应激组大鼠胸腺细胞Bcl-2蛋白表达阳性减弱、Bax蛋白阳性表达增强、TUNEL染色阳性细胞增多;实验1组Bcl-2蛋白表达阳性增强、Bax蛋白表达阳性减弱、TUNEL染色阳性细胞减少。结论西酞普兰可有效调节慢性应激大鼠的内分泌、免疫系统功能。并提示调节胸腺细胞Bcl-2/Bax蛋白表达水平、拮抗胸腺细胞凋亡是其重要途径之一。
Objective To investigate the effects of citalopram on blood glucose and immune system in chronic stress rats. Methods Thirty-two male SD rats were randomly divided into control group, stress group, experiment 1 group and experiment 2 group. Forced swimming was used to establish chronic stress model. Blood glucose, adrenal, thymus and spleen indexes were measured. The expression of Bcl-2 and Bcl-2 was detected by immunohistochemistry. Thymic cell apoptosis was detected by TUNEL. Results Compared with the stress group, the blood glucose in the control group decreased on the 20th day and the 29th day, while the blood glucose in the experimental group decreased on the 29th day (P <0.05). Compared with the control group, the blood glucose Increased (P <0.05). Compared with the stress group, the index of adrenal gland, thymus and spleen of rats in control group and experiment 1 group decreased (P <0.05). Compared with the control group, the index of thymus and spleen in experimental group 2 decreased (P <0.01). Compared with experimental group 1, the index of thymus and spleen in experimental group 2 decreased (P <0.05). The expression of Bcl-2 protein in thymocytes was weakened, the expression of Bax protein was increased and the number of TUNEL-positive cells was increased in the stress group. The expression of Bcl-2 protein in B group was increased, the expression of Bax protein was decreased and the number of TUNEL-positive cells was decreased. Conclusion Citalopram can effectively regulate the function of endocrine and immune system in chronic stress rats. It is suggested that the regulation of Bcl-2 / Bax protein expression in thymocytes and the inhibition of thymocyte apoptosis are two important pathways.