摘要
目的:研究不同剂量右美沙芬配伍曲马多术后镇痛对血清学指标的影响。方法:对80例接受腹部手术患者进行回顾性研究,包括接受20mg右美沙芬配伍曲马多镇痛方案的观察组40例以及接受10mg右美沙芬配伍曲马多术镇痛方案的对照组,采集血清后检测疼痛相关信号分子、炎症反应指标、应激反应指标、神经相关蛋白的含量。结果:(1)疼痛相关信号分子:观察组血清中JAK2、STAT3、STAT5、JNK、MCP-1的mRNA含量与对照组比较较低,差异有统计学意义(P<0.05);(2)炎症应激反应:观察组血清中白介素-17(IL-17)、白介素-23(IL-23)、高迁移率族蛋白1(HMGB1)、皮质醇(Cor)、去甲肾上腺素(NE)、肾上腺素(E)含量与对照组比较较低,差异有统计学意义(P<0.05);(3)神经相关蛋白:观察组血清中β-淀粉样蛋白(Aβ)、神经微管相关蛋白(Tau)、S100β的含量与对照组比较较低,差异有统计学意义(P<0.05)。结论:20mg右美沙芬配伍曲马多镇痛方案有助于抑制疼痛信号通路激活、缓解炎症应激反应、减轻神经元损伤,是理想的镇痛方案。
Objective： To study the effects of different doses of Dextromethorphan Hydrobromide combining with tramadol for postoperative analgesia on serum markers. Methods： 80 patients received abdominal surgery in our hospital were retrospectively studied, including 40 cases in observation group received 20 mg Dextromethorphan Hydrobromide combined with tramadol for analgesia, and 40 cases in control group received 10 mg Dextromethorphan Hydrobromide combined with tramadol for analgesia. Then serum were collected and pain related signal molecular, inflammatory response indicators, stress response indicators and nerve related protein contents were detected and compared. Results： （1）pain related signal molecules including mRNA contents of JAK2, STAT3, STATS, JNK, MCP-1 of observation group were lower compared with control group; （2） Inflammatory stress response indexes including IL-17, IL-23, HMGB-1, Cor, NE, E contents in serum of observation group patients were lower compared with control group; （3） Neural related protein： Aβ, Tau, S100L3 contents in serum of observa tion group patients were lower compared with control group. Conclusion.. 20 mg Dextromethorphan Hydrobromide combining with tramadol analgesia scheme is helpful to inhibit pain signaling pathway activation, reduce inflammation and stress re sponse, alleviate neuronal damage, it＇s an ideal analgesia scheme.
出处
《海南医学院学报》
CAS
2015年第7期988-990,994,共4页
Journal of Hainan Medical University
基金
江门市第二批科技计划项目(20067128)~~
关键词
右美沙芬
曲马多
信号通路
炎症应激反应
Dextromethorphan, Tramadol, Signaling pathways, Inflammation stress response
