Abstract: Objective To investigate the effect and mechanism of dexmedetomidine on hyperoxia-induced acute lung injury. Method Thirty male SD rats were randomly divided into blank control group, model group and dexmedetomidine group, and the hyperoxic lung injury model was constructed. The dexmedetomidine group was injected with dexmedetomidine daily while the control group and model group were injected with saline. The dry-wet weight proportion of lung tissue was measured. The expression levels of Il-6, iNOS, VEGF and bFGF in serum of rats were detected by ELISA. The expression levels of Il-2 and TNF were detected using semi-quantitative PCR. The Western blot was used to determine the protein expression of NLRP3 and Cav-1. Result The dry-wet weight proportion of lung tissue in the model group was (4.82±0.26), which was higher than that of the blank control group (2.29±0.51) and dexmedetomidine group (3.11±0.53), P<0.05. After 1 week of modeling, the mean respiratory rate of the dexmedetomidine group was(72.75±6.74)/min, which was lower than that of model group (P<0.05), and serum VEGF and bFGF levels were (0.368±0.079) ng/L and (24.85±2.36) ng/L, higher than those in model group (P<0.05). The levels of IL-6 and iNOS in the dexmedetomidine group were significantly lower than those in the model group, and NLRP3 and Cav-1 were significantly higher than those in the model group (P<0.05). Conclusion Dexmedetomidine can inhibit NLRP3 inflammatory activation and alleviate acute lung injury induced by high oxygen.

Key words: Dexmedetomidine, NLRP3 inflammatory body, hyperoxia, lung injury

摘要： 目的 探讨右美托咪定减轻高氧诱导的急性肺损伤的效果及机制。方法 雄性 SD 大鼠30只随机分为3组，即对照组，模型组与右美托咪定组，每组各10只，模型组与右美托咪定组构建高氧肺损伤模型。右美托咪定组在造模同时注射右美托咪定，对照组与模型组注射等量生理盐水。造模1周后取出肺部组织测定其干湿重比例。应用ELISA法检测大鼠血清中的IL-6、iNOS、VEGF和bFGF蛋白表达量。应用RT-PCR法测定IL-2 和TNFα表达量。应用免疫印迹Western blot法测定NLRP3和Cav-1蛋白表达量。结果 模型组肺组织干湿重比为(4.82±0.26)，高于对照组(2.29±0.51)和右美托咪定组(3.11±0.53)，P<0.05。在造模1周以后，右美托咪定组平均呼吸频率为(72.75±6.74)次/min，低于模型组(P<0.05)，血清VEGF和bFGF水平分别为(0.368±0.079) ng/L和(24.85±2.36) ng/L，高于模型组(P<0.05)。右美托咪定组IL-6和iNOS显著低于模型组，NLPR3和Cav-1则显著高于模型组(P<0.05)。结论 右美托咪定可以抑制NLRP3炎性体激活减轻高氧诱导的急性肺损伤。

关键词: 右美托咪定, NLRP3炎性体, 高氧性, 肺损伤