摘要
目的 评价脊髓驱动蛋白17（KIF17）在瑞芬太尼诱发切口痛大鼠痛觉过敏中的作用.方法 取尾静脉置管成功的雄性SD大鼠40只,2～3月龄,体重240～260 g,采用随机数字表法分为5组（n=8）：对照组（C组）静脉输注生理盐水1.5 ml 60 min;瑞芬太尼组（R组）静脉输注瑞芬太尼1 μg·kg-1·min-160 min;切口痛组（I组）建立切口痛模型,同时静脉输注生理盐水1.5 ml 60 min;瑞芬太尼＋切口痛组（R＋I组）制备切口痛模型的同时静脉输注瑞芬太尼1.5 ml 60 min;瑞芬太尼＋切口痛＋KIF17抑制剂组（R＋I＋M组）制备切口痛模型前30 min时,鞘内注射KIF17抑制剂Myr-Rc-1310 μg（溶于10 μl二甲基亚砜中）,制备切口痛模型同时静脉输注瑞芬太尼1 μg·kg-1·min-160 min.于输注瑞芬太尼或生理盐水前24 h、输注停止后2、6、24和48 h（T0-T4）时,测定机械缩足反应阈（MWT）和热缩足潜伏期（TWL）.于T4痛阈测定结束后处死大鼠,取脊髓组织,采用Western blot法测定脊髓KIF17和磷酸化KIF17（pKIF17）的表达水平.结果 与C组比较,R组、I组和R＋I组MWT降低,TWL缩短,脊髓KIF17和pKIF17表达上调（P〈0.05）;与R组和I组比较,R＋I组MWT降低, TWL缩短,脊髓KIF17和pKIF17表达上调（P〈0.05）;与I＋R组比较,R＋I＋M 组MWT升高,TWL延长,脊髓pKIF17和KIF17表达下调（P〈0.05）.结论 KIF17活性增加参与了瑞芬太尼诱发切口痛大鼠痛觉过敏的形成和维持.
Objective To evaluate the role of spinal kinesin superfamily motor protein 17 （KIF17）in remifentanil-induced hyperalgesia in rats with incisional pain. Methods Forty male Sprague-Dawley rats, aged 2-3 months, weighing 240-260 g, were divided into 5 groups（n=8 each）using a random number table： control group（group C）, remifentanil group（group R）, incisional pain group （group I）, remifentanil plus incisional pain group（group R＋I）and remifentanil plus incisional pain plus KIF17 inhibitor group（group R＋I＋M）. Normal saline 15 ml was intravenously infused for 60 min in group C. Remifentanil 1 μg·kg-1·min-1was intravenously infused for 60 min in group R. In group I, in-cisional pain model was established, and normal saline 15 ml was intravenously infused for 60 min at the same time. In group R＋I, incisional pain model was established, and remifentanil 15 ml was intravenous-ly infused for 60 min at the same time. In group R＋I＋M, KIF17 inhibitor Myr-Rc-13 10 μg（in 10 μl dimethyl sulfoxide）was injected intrathecally, and remifentanil 1 μg·kg-1·min-1was intravenously in-fused for 60 min while incisional pain model was established. The mechanical paw withdrawal threshold （MWT）and thermal paw withdrawal latency（TWL）were measured at 24 h before remifentanil or normal saline infusion and at 2, 6, 24 and 48 h after the end of infusion. The rats were sacrificed after the last measurement of pain threshold, and the lumbar segment of the spinal cord was removed for determination of the expression of KIF17 and phosphorylated KIF17（pKIF17）by Western blot. Results Compared with group C, MWT was significantly decreased, TWL was shortened, and the expression of KIF17 and pKIF17 was up-regulated in R, I and R＋I groups（P〈0.05）. Compared with R and I groups, MWT was signifi-cantly decreased, TWL was shortened, and the expression of KIF17 and pKIF17 was up-regulated in group R＋I（P〈0.05）. Compared with group I＋R, MWT was significantly increased, TWL was prolonged, and the expression of KIF17 and pKIF17 was down-regulated in group R＋I＋M（P〈0.05）. Conclusion In-creased activity of KIF17 is involved in the development and maintenance of remifentanil-induced hyperalge-sia in rats with incisional pain.
出处
《中华麻醉学杂志》
CSCD
北大核心
2017年第10期1226-1229,共4页
Chinese Journal of Anesthesiology
基金
国家自然科学基金（81371245,30972847）
关键词
哌啶类
疼痛
手术后
痛觉过敏
驱动蛋白
脊髓
Piperidines
Pain,postoperative
Hyperalgesia
Kinesin
Spinal cord
