摘要
目的探讨p38丝裂原活化蛋白激酶(p38 MAPK)信号通路在依达拉奉影响单肺通气患者炎症细胞因子白细胞介素(IL)-6和IL-10中的作用。方法将40例择期拟进行肺叶切除术肺癌患者随机分为对照组20例和试验组20例。2组患者均静脉注射0.03 mg·kg-1咪唑安定、3μg·kg-1芬太尼,吸入8%七氟醚麻醉诱导。麻醉诱导后,试验组给予0.5 mg·kg-1依达拉奉加入0.9%氯化钠注射液100 mL,静脉滴注;对照组给予等量0.9%氯化钠注射液。2组麻醉维持用药相同,均在麻醉后切皮前(T0)、膨肺后60 min(T1)、术后1 h(T2)测定磷酸化p38 MAPK(p-p38 MAPK)、p38 MAPK表达水平和IL-6、IL-10血浆浓度;p-p38 MAPK和p38 MAPK比值反映p38 MAPK激活程度;IL-6/IL-10比值反映促炎和抗炎细胞因子平衡状态。结果与T0比较,2组p38 MAPK、p-p38 MAPK表达水平、p38 MAPK激活程度和IL-6血浆浓度、IL-6/IL-10比值于T1、T2均明显上升(P<0.05)。与对照组比较,试验组血浆p38 MAPK、p-p38 MAPK表达水平、p38 MAPK激活程度和IL-6血浆浓度、IL-6/IL-10比值于T1、T2均显著降低(P<0.05)。结论 p38 MAPK信号通路参与依达拉奉抑制单肺通气患者机体促炎性细胞因子的生成和释放,维持促炎性/抗炎性细胞因子的相对平衡。
Objective To investigate the role of p38 mitogen-activated protein kinase（ p38 MAPK） in edaravone influencing cytokine IL-6 and IL-10 on patients undergoing one lung ventilation.Methods Forty patients with lung cancer undergoing elective lung resection were randomly divided into control group （ n =20 ） and treatment group （ n =20 ）.Anesthesia was induced with midazolam 0.03 mg · kg-1 , fentanyl 3 μg· kg -1 and 8% sevoflurane.Patients in edaravone group received edaravone 0.5 mg · kg-1 after induction of anesthesia, while those in control group were given 0.9%NaCl of the same volume.Blood sample were taken and detected before skin incision （ T0 ） , 60 min after lungs inflated（ T1 ） and 1 h after surgery （ T2 ） for expression of phosphorylated p38 MAPK （ p -p38 MAPK ） , p38 MAPK and plasma concentration of interleukin-6（IL-6）.The ratio between p-p38 MAPK and p38 MAPK was calculated.Results Compared with T0 , the data of p38 MAPK, p-p38 MAPK, p-p38 MAPK /p38 MAPK ratio and IL-6 concentration,＆amp;nbsp;IL-6/IL-10 ratio were all significantly increased at T1and T2（P〈0.05）.And those in treatment group were signifi-cantly lowered than those in control group at T1 and T2 （ P〈0.05）.Conclusion p38 MAPK signal pathway is involved in edaravone inhibiting proinflammatory cytokine and maintaining a relative stability of proinflammatory/anti -inflammatory cytokine in patients undergoing one lung ventilation.
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2015年第9期683-685,698,共4页
The Chinese Journal of Clinical Pharmacology
基金
青岛市科技局课题民生科技计划基金项目(13-1-3-2-nsh)
