Park Jung Hyun, Cho Seung Hee, Kim Rip, Na Sang Hoon, Kang Eun-Sun, Yeom Mi-Young, Jang Yeon
Department of Anesthesiology and Pain Medicine, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Incheon, Korea.
Department of Anesthesiology and Pain Medicine, Catholic Medical Center, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Korean J Pain. 2021 Apr 1;34(2):185-192. doi: 10.3344/kjp.2021.34.2.185.
It is known that some analgesics as well as pain can affect the immune system. The aim of this study was to investigate the analgesic effect and immunomodulation of pregabalin (PGB) in a mouse incisional pain model.
A postoperative pain model was induced by hind paw plantar incision in male BALB/c mice. Mice were randomly divided into four groups (n = 8): a saline-treated incision (incision), PGB-treated incision (PGB-incision), sham controls without incision or drug treatment (control), and a PGB-treated control (PGB-control). In the PGB treated groups, PGB was administered intraperitoneally (IP) 30 minutes before and 1 hour after the plantar incision. Changes of the mechanical nociceptive thresholds following incision were investigated. Mice were euthanized for spleen harvesting 12 hours after the plantar incision, and natural killer (NK) cytotoxicity to YAC 1 cells and lymphocyte proliferation responses to phytohemagglutinin were compared among these four groups.
Mechanical nociceptive thresholds were decreased after plantar incision and IP PGB administration recovered these decreased mechanical nociceptive thresholds ( < 0.001). NK activity was increased by foot incision, but NK activity in the PGB-incision group was significantly lower than that in the Incision group ( < 0.001). Incisional pain increased splenic lymphocyte proliferation, but PGB did not alter this response.
Incisional pain alters cell immunity of the spleen in BALB/c mice. PGB showed antinocieptive effect on mouse incisional pain and attenuates the activation of NK cells in this painful condition. These results suggest that PGB treatment prevents increases in pain induced NK cell activity.
已知某些镇痛药以及疼痛会影响免疫系统。本研究旨在探讨普瑞巴林(PGB)在小鼠切口疼痛模型中的镇痛作用和免疫调节作用。
通过雄性BALB/c小鼠后爪足底切口诱导术后疼痛模型。将小鼠随机分为四组(n = 8):生理盐水处理的切口组(切口组)、PGB处理的切口组(PGB-切口组)、未进行切口或药物处理的假手术对照组(对照组)和PGB处理的对照组(PGB-对照组)。在PGB处理组中,在足底切口前30分钟和切口后1小时腹腔内注射(IP)PGB。研究切口后机械性伤害感受阈值的变化。足底切口12小时后对小鼠实施安乐死以获取脾脏,比较这四组对YAC 1细胞的自然杀伤(NK)细胞毒性以及对植物血凝素的淋巴细胞增殖反应。
足底切口后机械性伤害感受阈值降低,腹腔注射PGB可使降低的机械性伤害感受阈值恢复(<0.001)。足部切口使NK活性增加,但PGB-切口组的NK活性显著低于切口组(<0.001)。切口疼痛增加脾脏淋巴细胞增殖,但PGB未改变此反应。
切口疼痛改变BALB/c小鼠脾脏的细胞免疫。PGB对小鼠切口疼痛显示出镇痛作用,并减弱了这种疼痛状态下NK细胞的激活。这些结果表明,PGB治疗可防止疼痛诱导的NK细胞活性增加。