卡托普利对烟雾吸入性损伤大鼠肺的保护作用

Protective effects of captopril on smoke inhalation injury in rats

目的:探讨卡托普利对烟雾吸入性损伤大鼠肺的保护作用。方法:雄性SD大鼠48只,随机分为对照组、致伤组、卡托普利组。卡托普利组烟雾吸入性致伤后腹腔注射卡托普利,致伤组致伤后注射与卡托普利组等体积的生理盐水,对照组不做致伤处理。检测各组肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、超氧化物歧化酶(SOD)、丙二醛(MDA)和髓过氧化物酶(MPO)的水平。并取各组5 h大鼠左肺组织行病理切片光镜观察。结果:光镜下对照组肺泡结构清晰完整;致伤组肺组织肺泡间质增宽、炎细胞浸润;卡托普利组肺组织炎细胞较致伤组减少。卡托普利组各时相点血清TNF-α和IL-6含量高于对照组(P<0.01),但低于致伤组(P<0.05)。致伤组IL-10含量与对照组相比无差异(P>0.05),卡托普利组IL-10含量高于对照组(P<0.01)。卡托普利组各时相点肺组织MDA和MPO含量均高于对照组(P<0.01),但低于致伤组(P<0.05)。卡托普利组5 h肺组织SOD含量高于致伤组(P<0.05),但仍低于对照组(P<0.01)。结论:卡托普利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 captopril on smoke inhalation injury in rats.Methods： Forty-eight rats were randomly assigned to three groups：control group,injury group and captopril group.The captopril group were administered i.p.captopril after inhalation injury,with the same volume the injury group were administered i.p.normal saline.Then each group was examined for tumor necrosis factor-α（TNF-α）,interleukin-6（IL-6）,interleukin-10（IL-10）,superoxide dismutase（SOD）,malondialdehyde（MDA） and myeloperoxidase（MPO）.The left lung tissues of each group at 5 h were examined under an optical microscope.Results： The lung in the captopril group was found to have inflammatory granulocytes and edema compared with the control group under microscope,which was better than injury group.The TNF-α and IL-6 levels of captopril group were higher than those of the control group（P0.01）,and were lower than those of the injury group（P0.05）.The IL-10 levels of injury group had no difference with that of control group,while captopril group was higher than that of control group（P0.01）.The MDA and MPO levels of captopril group were higher than those of the control group（P0.01）,and were lower than those of the injury group（P0.05）.The SOD levels of captopril group at 5 h were higher than that of injury group（P0.05）,but were still lower than that of control group（P0.01）.Conclusion： Captopril has some protective effects on smoke inhalation injured rats by decreasing the inflammatory response.