胰岛素对烟雾吸入性损伤大鼠肺的保护作用

Protective effects of insulin on smoke inhalation injury in rats' model

目的探讨胰岛素对烟雾吸入性损伤大鼠肺的保护作用。方法雄性Wistar大鼠54只,随机分为正常组、盐水组、胰岛素组,每组18只。胰岛素组烟雾吸入性致伤后,皮下注射胰岛素(5U/Kg),盐水组致伤后注射与胰岛素组等体积的生理盐水,正常组不做致伤处理。三组大鼠分别于12h、24h、48h尾静脉取血检测血糖水平后腹主动脉取血2ml,离心取血清检测肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)含量,并取各组各时段大鼠肺组织行病理切片光镜观察。结果光镜下正常组肺泡结构清晰完整;盐水组肺组织肺泡间隔增宽、炎细胞浸润;胰岛素组肺组织炎细胞较盐水组减少。与正常组比较,盐水组12h血糖水平升高(P<0.01),与盐水组比较,胰岛素组各时相点血糖水平降低(P<0.01)。胰岛素组不同时相点TNFα和IL-6含量高于正常组(P<0.01)但低于盐水组(P<0.05或P<0.01)。盐水组IL-10含量与正常组相比无统计学差异(P>0.05),胰岛素组IL-10含量与正常组相比升高(P<0.01)。结论胰岛素可减轻烟雾吸入性损伤大鼠体内炎性反应,对肺组织有一定的保护作用。

Objective To investigate the protective effects of insulin on smoke inhalation injury in rats . Methods Fifty-four rats were randomly assigned to three groups ： control group, saline group and insulin group. The insulin group were subcutaneously injected 5 U/kg insulin after inhalation injury, the saline group were injected the same volume normal saline. At12 h, 24 h and 48 h, blood glucose was decteted. Arterial blood was collected and the levels of tumor necrosis factor-α （TNF-α）, interleukin-6 （IL-6） and interleukin-10（IL-10） were determined. The lung tissues were examined under microscope. Results The lung of the saline group was found to have inflammatory granulocytes compared with the control group under microscope, the exudation and edema of insulin group were improved compared with the saline group. Compared with the control group, the blood glucose of saline group was higher at 12 h（P〈0.01）. The blood glucose of insulin group was lower than the saline group at every phase. Compared with the control group, the TNF a and IL-6 levels were higher in the insulin group and saline group （P〈0.01）. The TNF-α and IL-6 level of insulin group were lower than the saline group （P〈 0.05 or P〈 0.01）. There were no significant differences of IL-10 between saline group and control group （P〉 0.05）. The IL-10 levels of insulin group was higher than the control group （P〈 0.01）. Conclusion Insulin has some protective effects on smoke inhalation injured rats by decreasing the inflammatory response.