右美托咪定在脂多糖诱导急性肺损伤小鼠中对JAK2/STAT3通路影响及意义分析

目的：探讨分析右美托咪定在脂多糖诱导急性肺损伤小鼠中对JAK2/STAT3通路影响及意义分析。方法：将实验室120例健康小鼠作为研究对象，采用随机数字表法分为对照、观察两组，每组60只小鼠，其中对照组小鼠静脉给予10mg/kg脂多糖后即可给予生理盐水5mg/kg，观察组小鼠静脉给予10mg/kg脂多糖后即可给予右美托咪定10mg/kg，比较两组急性肺损伤小鼠蛋白酪氨酸激酶/转录信号传导子和激活子3（JAK2/STAT3）通路与右美托咪定应用与否的关系及影响。结果：两组小鼠治疗前Murray肺损伤评分情况无明显差异，无统计学意义（P﹥0.05）。采用右美托咪定治疗的观察组小鼠肺损伤评分情况明显优于对照组小鼠，差异有统计学意义（P＜0.05）；经对比观察，观察组小鼠雷帕霉素靶蛋白（mTOR）（0.47±0.12）mg/L及雷帕霉素靶蛋白磷酸化（p-mTOR）（0.56±0.15）mg/L水平均优于对照组mTOR（0.37±0.10）mg/L及p-mTOR水平（0.32±0.09）mg/L，差异有统计学意义（P＜0.05）。观察组与对照组小鼠微管相关蛋白（LC3-Ⅱ）水平相近且无明显差异，无统计学意义（P﹥0.05）。结论：急性肺损伤小鼠静脉注射右美托咪定后，肺损伤评分较低，小鼠JAK2/STAT3通路各项生理参数趋于正常，右美托咪定通过抑制JAK2/STAT3通路起到对肺脏的保护作用。

Effect and significance of Dexmedetomidine on JAK2/STAT3 pathway in mice with lipopolysaccharide-induced acute lung injury

Objective: To investigate and analyze the effect and significance of Dexmedetomidine on JAK2/STAT3 pathway in lipopolysaccharide-induced acute lung injury mice. Methods: One hundred and twenty healthy laboratory mice were included in this study and were randomly divided into control group and observation group, with 60 mice in each group. Mice in the control group were intravenously administered with saline 5mg/kg immediately after 10 mg/kg lipopolysaccharide, while mice in the observation group were given 10 mg/kg Dexmedetomidine immediately after 10 mg/kg lipopolysaccharide. Correlation between JAK2/STAT3 pathway and Dexmedetomidine application was were compared in the two groups. Results:Murray lung injury score showed no significant difference in the two groups before treatment, without significant difference (P﹥0.05). After Dexmedetomidine treatment, lung injure score in the observation group was obviously better than that in the control group, with significant difference (P<0.05). Mammalian target of rapamycin (0.47 ±0.12)mg/L and mammalian target of rapamycin phosphorylation (0.56 ±0.15)mg/L in the observation group were significantly higher than that in the control group(0.37±0.10)mg/L and(0.32±0.09)mg/L(P<0.05). There was no significant difference in the microtubule-associated protein (LC3-II) levels between the two groups (P﹥0.05). Conclusion: Intravenous injection of Dexmedetomidine lowers lung injury score in acute lung injury mice, JAK2/STAT3 pathway physiological parameters tend to the normal, Dexmedetomidine inhibits JAK2/STAT3 pathway and thus plays protective effects on the lungs.