摘要
目的探讨盐酸羟考酮对脊髓损伤大鼠氧化应激的影响及神经性病理疼痛的作用。方法30只SD大鼠随机分为假手术组(Sham组)、脊髓损伤模型组(SCI组)和盐酸羟考酮组(OHI组),Allen’s方法建立脊髓损伤大鼠模型。于实验开始前1d及造模后1d、3d、7d、14d对各组大鼠进行BBB评分,进行热缩爪潜伏期和机械性缩爪潜伏期的测定;利用HE染色观察脊髓损伤病理变化;免疫荧光法检测活性氧ROS的表达;ELISA检测血清中SOD、MDA、GSH-PX的含量;TUNEL法检测细胞凋亡情况;Western blot法检测Nrf2、Keap1、HO-1的表达水平。结果盐酸羟考酮抑制SCI大鼠病理损伤,缓解神经病理性疼痛,抑制ROS的释放,抑制MDA的分泌,促进SOD、GSH-PX的释放,上调Nrf2、HO-1的表达,下调Keap1的表达。结论盐酸羟考酮通过激活Nrf2/Keap1/HO-1信号通路抑制氧化应激,缓解SCI大鼠神经病理性头痛,降低病理损伤。
Objective To explore the effect of oxycodone hydrochloride on oxidative stress and neuropathic pain in rats with spinal cord injury.Methods 30 SD rats were randomly divided into sham operation group(Sham group),spinal cord injury model group(SCI group),and oxycodone hydrochloride group(OHI group).The spinal cord injury rat model was established by Allen’s method.1d before the experiment and 1d,3d,7d,14d after modeling,the rats in each group were scored by BBB method,and the latent period of heat shrinking paw and mechanical paw shrinking were measured.The pathological changes of spinal cord injury were observed by HE staining.The expression of reactive oxygen species(ROS)was detected by immunofluorescence assay.The contents of SOD,MDA and GSH-Px in serum were detected by ELISA.Apoptosis was detected by TUNEL assay.The expression of Nrf2,Keap1 and HO-1 were detected by Western blot.Results Oxycodone hydrochloride inhibited pathological damage in SCI rats,relieved neuropathic pain,inhibited the release of ROS,inhibited the secretion of MDA,promoted the release of SOD and GSH-PX,up-regulated the expression of Nrf2 and HO-1,and down-regulated the expression of Keap1.Conclusion Oxycodone hydrochloride inhibits oxidative stress by activating the Nrf2/Keap1/HO-1 signaling pathway,relieves neuropathic headache in SCI rats,and reduces pathological damage.
作者
孙玥
孙晓峰
焦晶华
金允淑
SUN Yue;SUN Xiao-feng;JIAO Jing-hua;JIN Yun-shu(Department of Anesthesiology,Affiliated Central Hospital of Shenyang Medical College,Shenyang 110024,China)
出处
《解剖科学进展》
CAS
2022年第5期527-530,534,共5页
Progress of Anatomical Sciences
基金
辽宁省自然科学基金(2018011490-301)。
