TRPA1参与挤压损伤诱导神经病理性疼痛的形成及其机制  

Involvement of TRPA1 in formation of crush injury induced neuropathic pain and its mechanism

作　　者：霍苗[1] 白宁[1] 王晖[1] 徐瑞芬[1] 郑星星[1] 赵紫玉 杨光[1] 郭姣[1] Huo Miao;Bai Ning;Wang Hui;Xu Ruifen;Zheng Xingxing;Zhao Ziyu;Yang Guang;Guo Jiao(Department of Anesthesiology,Shaanxi Provincial People’s Hospital,Xi’an 710068,China)

机构地区：[1]陕西省人民医院麻醉科,西安710068

出　　处：《中华生物医学工程杂志》2022年第5期558-562,共5页Chinese Journal of Biomedical Engineering

摘　　要：分析TRPA1的激活参与挤压损伤诱导神经病理性疼痛的形成及其机制。给药2 h及给药4 h时模型+干预组小鼠热缩足潜伏期明显高于模型组,冷痛评分明显低于模型组,且差异存在统计学意义( P<0.05);给药2 h及给药4 h时模型+干预组小鼠脑组织TRPA1蛋白水平明显低于模型组,且差异存在统计学意义( P<0.05)。TRPA1的激活在挤压损伤诱导神经病理性疼痛的形成过程中起到重要的调节和传递作用。The purpose of this study was to investigate whether activation of TRPA1 is involved in the formation of crush injury induced neuropathic pain and its mechanism.At 2 h and 4 h after administration of TRPA1 inhibitor,mice models presented significantly longer paw withdrawal thermal latency and lower cold pain ratings compared with those without intervention(P<0.05).Compared with those without intervention,the levels of TRPA1 protein in brain tissue of mice model were significantly lower at 2 h and 4 h of administration,with statistically significant difference(P<0.05).In summary,activation of TRPA1 plays an important role in regulation and transmission of neuropathic pain induced by crush injury.

关 键 词：TRPA1 损伤 神经病理性疼痛 激活 

分 类 号：R741[医药卫生—神经病学与精神病学]