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目的:探讨在大鼠乳腺癌骨转移诱导癌症疼痛的调控过程中Akt信号通路的作用。方法:将Wistar成模wistar大鼠随机分为Model组、Model+GSK690693组及Model+Saline组;Model组大鼠不进行鞘内注射,Model+GSK690693组及Model+Saline组大鼠,于手术后数天(post-cancer cell implantation day,PID)PID 13 d、14 d及21 d鞘内分别注入Akt特异抑制剂GSK690693、等量生理盐水组,分别于PID 0 d、7 d、14 d及21 d,观察大鼠痛相关行为学检查,PID 21 d取DRG行免疫印迹检查p-Akt表达。结果:在鞘内注射Akt特异性抑制剂GSK690693后,Model+GSK690693组大鼠的机械缩足反射阈值上升,自发性疼痛行为值及患侧DRG中p-Akt表达下降。在PID 14 d、21 d等不同时间节点,Model+GSK690693组大鼠的疼痛行为学与Model+Saline组大鼠、Model组大鼠经统计学比较有显著的统计学差异(P<0.01);PID 21d Model+GSK690693组大鼠患侧DRG中p-Akt表达与Model组的比较有显著统计学意义(P<0.01),与Model+Saline组比较有统计学意义(P<0.05);结论:鞘内注射Akt特异性抑制剂GSK690693可抑制大鼠乳腺癌骨转移诱导的大鼠痛相关行为。
AIM: To investigate the role of Akt signaling in the regulation of cancer pain induced by bone metastasis of breast cancer in rats. Methods: Wistar rats were randomly divided into Model group, Model + GSK690693 group and Model + Saline group. Model rats were not intrathecally injected with Model + GSK690693 and Model + Saline rats. After operation The animals were injected intrathecally with Akt-specific inhibitor GSK690693, an equal volume of normal saline on days 13, 14, and 21 after PID control, respectively on day 0, day 7 and day 14 after PID control d, Observe the pain-related behavioral examination in rats, PID 21 d to take DRG line immunoblot to examine p-Akt expression. Results: After intrathecal administration of Akt specific inhibitor GSK690693, the mechanical reflex threshold of Model + GSK690693 rats increased, and the values of spontaneous pain and the expression of p-Akt in DRG decreased. The pain behavior of Model + GSK690693 group was significantly different from that of Model + Saline group and Model group (P <0.01) at the different time points of PID 14 d and 21 d. The expression of p-Akt in ipsilateral DRG of PID 21d Model + GSK690693 group was significantly higher than that of model group (P <0.01), and the difference was statistically significant (P <0.05) with Model + Saline group.Conclusion: Intrathecal injection of Akt specific inhibitor GSK690693 can inhibit pain-related behavior induced by bone metastasis in rats with breast cancer.