摘要
目的研究鞘内注射布托啡诺对大鼠急性疼痛时血清细胞因子水平的影响,探讨鞘内注射布托啡诺治疗急性疼痛的机制。方法取清洁级SD雄性成年大鼠45只,随机数字表法分为空白组、对照组与布托啡诺组,每组15只;每组再平均分为3个亚组,每亚组5只。空白组不实施任何手术;对照组及布托啡诺组制造慢性缩窄性损伤模型及鞘内置管后,分别鞘内注射生理盐水10μl及布托啡诺24μg。3组分别自内眦取血,双抗体夹心酶联免疫吸附法检测血清白细胞介素(IL)-6与IL-10水平。结果术后48h内对照组和布托啡诺组IL-6水平均高于术前,差异有统计学意义(P〈0.05或P〈0.01);对照组IL-6在术后6h达峰值[(114.35±9.04)ng/L],而布托啡诺组的峰值[(40.55±5.97)ng/L]延迟到术后12h,且布托啡诺组各时点的IL-6均低于对照组,差异有统计学意义(均P〈0.01)。对照组血清IL-10水平在术后12h开始高于术前,布托啡诺组则均在术后9h开始高于术前,且术后9~48h各时点布托啡诺组IL-10水平均高于对照组,差异有统计学意义(均P〈0.01)。对照组血清IL-10水平在术后18h达峰值[(29.53±3.14)ng/L],布托啡诺组血清IL-10水平在术后15h达峰值[(50.39±2.74)ng/L]。结论鞘内注射布托啡诺可降低IL-6水平,并明显增高IL-10水平,并阻断IL-6恶性循环,延缓疼痛高峰时相及增高疼痛阈值,促进促/抑炎症细胞因子平衡的恢复。
Objective To measure serum IL-6 and IL-10 in acute painful rats of intrathecal butorphanol and to investigate theraputic mechanisms of butorphanol on acute pain. Methods Fourty-five healthy male SD rats were randomly divided into three groups. Every group was equally divided into three subgroups with5 animals in each subgroup. Group B accepted the same basic anesthesia without any operation and blood was obtained from epicathus of rats. Group C received intrathecal normal saline 10μl after CCI. Group T received intrathecal butorphanol 24μg after CCI. In subgroup 1 blood samples were drawn from epicathus before the CCI, 9 hours, 18 hours after CCI. Similarly, blood samples in subgroup 2 were obtained at hours 3, 12, 24 while subgroup3 on hour6, 15,48, respectively. Serum IL-6 and IL-10 in each sample were measured by enzyme linked immunosorbent assay. Results Serum IL-6 in group C and group T within 48 hours after CCI increased after operation. In group C, the peak time of serum IL-6 was 6 hours after operation with 12 hours in group T. The serum IL-6 in group T were lower than that in group C at the same time point. Serum IL-10 in group C began to increase 12 hours after CCI. Serum IL-10 production in group C reached peak value at 18h after CCI, with 15h in group T. Conclusion Intrathecal butorphanol decreases the level of serum IL-6 and increases serum IL-10, accelerating the balance of promotion or inhibitor inflammatory factors.
出处
《中国医药》
2009年第2期84-86,共3页
China Medicine
基金
基金项目:山东省自然基金资助课题(Y2006C105)