褪黑素对糖尿病合并创伤应激大鼠脾淋巴细胞免疫功能的影响

Effects of Melatonin on the Immune Functions of Diabetic Rats Combined with Injury-induced Stress

目的 :研究褪黑素对创伤应激状态下糖尿病大鼠脾淋巴细胞免疫功能的影响。方法 :四氧嘧啶诱导的糖尿病大鼠给予 17d褪黑素处理 ,采用MTT法、ELISA法分别检测褪黑素对糖尿病大鼠创伤应激前后脾淋巴细胞增殖反应和ConA诱生的脾淋巴细胞TNF α、IL 6分泌水平的变化。设正常对照组、糖尿病对照组、糖尿病 +溶媒组作为对照。结果 :每日腹腔注射 0 1mg/kg的褪黑素可显著改善糖尿病及糖尿病合并创伤应激大鼠低下的脾淋巴细胞增殖反应 ,降低ConA诱生的脾淋巴细胞TNF α、IL 6的分泌水平 ;每日腹腔注射 0 2mg/kg的褪黑素可显著抑制糖尿病及糖尿病合并创伤应激大鼠的脾淋巴细胞增殖反应 ,提高ConA诱生的脾淋巴细胞TNF α、IL 6分泌水平。结论 :褪黑素对糖尿病及糖尿病合并创伤应激大鼠低下的脾淋巴细胞免疫功能有调节作用 ,褪黑素剂量为每日 0 1mg/kg时对机体脾淋巴细胞免疫功能有保护作用 ,而褪黑素剂量为每日 0 2mg/kg时可抑制上述动物模型的脾淋巴细胞免疫功能。

AIM:To investigate the effects of melatonin on spleen lymphocyte proliferating response,secretion levels of TNF-α,IL-6 induced by Con A in alloxan-induced diabetes combined with injury-induced stress of rats model.METHOD:Male SD rats(weighed 200±20 g) were divided into 5 groups:(1)normal control group;(2)DM control group;(3)DM+vehicle group;(4)DM+M1 group(melatonin 0.1 mg·kg -1·d -1,ip consecutive 17 d);and(5)DM+M2 group(melatonin 0.2 mg·kg -1·d -1,ip consecutive 17 d). By means of MTT,ELISA,the variations of lymphocyte proliferating response,Con A induced TNF-α,IL-6 secretion levels were observed at the spots of before stress(injury-induced),and after stress 1,12,72 h respectively.RESULT:The dosage of 0.1 mg·kg -1·d -1 melatonin could improve the spleen lymphocyte proliferating response,and decrease the secretion levels of TNF-α,IL-6 induced by Con A in diabetic rats combined with or without injury-induced stress.The dosage of 0.2 mg·kg -1·d -1 melatonin could inhibit the spleen lymphocyte proliferating response,and elevate the secretion levels of TNF-α,IL-6 induced by Con A in diabetic rats combined with or without injury-induced stress.CONCLUSION:The impaired cellular immunity in diabetic rats combined with or without injury-induced stress could be modulated by the dosage of 0.1 mg·kg -1·d -1 melatonin intraperitoneally,After melatonin 0.2 mg·kg -1·d -1 intraperitoneally,there was significant inhibition of cellular immunity to be observed in diabetic rats combined with or without injury-induced stress.