脊髓趋化因子受体2介导大鼠骨癌痛维持的机制研究

R338.8; 目的·研究脊髓趋化因子受体2(chemokine C-C motif receptor 2,CCR2)介导大鼠骨癌痛(bone cancer pain,BCP)维持的机制.方法·选取54只SD大鼠为研究对象,将其分为BCP组、假手术组、BCP+INCB3344(CCR2特异性阻断剂)组和BCP+溶剂对照组.向BCP组大鼠胫骨骨髓腔内注入Walker256乳腺癌细胞,建立骨癌痛模型;假手术组则注射等量的生理盐水.BCP+INCB3344组是在BCP模型建立第14日后,向大鼠鞘内注射INCB3344;BCP+溶剂对照组则注射等量的溶剂.通过检测BCP组大鼠和假手术组大鼠的机械痛阈值...

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Published in上海交通大学学报（医学版） Vol. 39; no. 11; pp. 1261 - 1267
Main Authors 王丽娅, 高坡, 周晔
Format Journal Article
LanguageChinese
Published 上海交通大学医学院附属国际和平妇幼保健院产科,上海市胚胎源性疾病重点实验室,上海市临床重点专科(建设项目)-"强主体"妇产科,上海 200030%上海交通大学医学院附属仁济医院麻醉科,上海,200127 28.11.2019
Subjects
趋化因子受体2
脊髓
自发兴奋性突触后电流
骨癌痛
胶状质层
Online AccessGet full text
ISSN1674-8115
DOI10.3969/j.issn.1674-8115.2019.11.008

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Abstract R338.8; 目的·研究脊髓趋化因子受体2(chemokine C-C motif receptor 2,CCR2)介导大鼠骨癌痛(bone cancer pain,BCP)维持的机制.方法·选取54只SD大鼠为研究对象,将其分为BCP组、假手术组、BCP+INCB3344(CCR2特异性阻断剂)组和BCP+溶剂对照组.向BCP组大鼠胫骨骨髓腔内注入Walker256乳腺癌细胞,建立骨癌痛模型;假手术组则注射等量的生理盐水.BCP+INCB3344组是在BCP模型建立第14日后,向大鼠鞘内注射INCB3344;BCP+溶剂对照组则注射等量的溶剂.通过检测BCP组大鼠和假手术组大鼠的机械痛阈值来判断鉴定BCP模型是否成功.采用蛋白质印迹检测假手术组和BCP组大鼠脊髓后角CCR2表达情况.通过机械痛行为的测试,观察鞘内给予INCB3344对BCP模型大鼠机械痛阈的影响.通过全细胞膜片钳记录观察BCP组、BCP+INCB3344组和BCP+溶剂对照组大鼠脊髓胶状质层(substantia gelatinosa,SG)神经元自发兴奋性突触后电流(spontaneous excitatory postsynaptic currents,sEPSCs)、α-氨基-3-羟基-5-甲基-4-异唑丙酸(α-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid,AMPA)电流和N-甲基-D-天冬氨酸(N-methyl-D-aspartic acid,NMDA)电流间的差异.结果·与假手术组相比,术后14 d时BCP组大鼠的机械痛阈下降且术侧脊髓后角CCR2的表达增加(P=0.000,P=0.009),而鞘内注射INCB33444 h时可显著升高BCP大鼠的机械痛阈(P=0.002).BCP组大鼠SG神经元sEPSCs的频率和幅度、AMPA电流和NMDA电流幅度均高于假手术组(均P=0.000),而鞘内给予INCB3344可显著抑制BCP大鼠的上述指标(均P<0.05);此外,胞外给予INCB3344也可显著抑制BCP大鼠SG神经元sEPSCs的频率(P=0.001)和幅度(P=0.020).结论·脊髓后角的CCR2可通过增强AMPA和NMDA受体功能来介导BCP大鼠脊髓后角兴奋性突触传递效能的增强,该作用可能是BCP维持的重要机制.
AbstractList R338.8; 目的·研究脊髓趋化因子受体2(chemokine C-C motif receptor 2,CCR2)介导大鼠骨癌痛(bone cancer pain,BCP)维持的机制.方法·选取54只SD大鼠为研究对象,将其分为BCP组、假手术组、BCP+INCB3344(CCR2特异性阻断剂)组和BCP+溶剂对照组.向BCP组大鼠胫骨骨髓腔内注入Walker256乳腺癌细胞,建立骨癌痛模型;假手术组则注射等量的生理盐水.BCP+INCB3344组是在BCP模型建立第14日后,向大鼠鞘内注射INCB3344;BCP+溶剂对照组则注射等量的溶剂.通过检测BCP组大鼠和假手术组大鼠的机械痛阈值来判断鉴定BCP模型是否成功.采用蛋白质印迹检测假手术组和BCP组大鼠脊髓后角CCR2表达情况.通过机械痛行为的测试,观察鞘内给予INCB3344对BCP模型大鼠机械痛阈的影响.通过全细胞膜片钳记录观察BCP组、BCP+INCB3344组和BCP+溶剂对照组大鼠脊髓胶状质层(substantia gelatinosa,SG)神经元自发兴奋性突触后电流(spontaneous excitatory postsynaptic currents,sEPSCs)、α-氨基-3-羟基-5-甲基-4-异唑丙酸(α-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid,AMPA)电流和N-甲基-D-天冬氨酸(N-methyl-D-aspartic acid,NMDA)电流间的差异.结果·与假手术组相比,术后14 d时BCP组大鼠的机械痛阈下降且术侧脊髓后角CCR2的表达增加(P=0.000,P=0.009),而鞘内注射INCB33444 h时可显著升高BCP大鼠的机械痛阈(P=0.002).BCP组大鼠SG神经元sEPSCs的频率和幅度、AMPA电流和NMDA电流幅度均高于假手术组(均P=0.000),而鞘内给予INCB3344可显著抑制BCP大鼠的上述指标(均P<0.05);此外,胞外给予INCB3344也可显著抑制BCP大鼠SG神经元sEPSCs的频率(P=0.001)和幅度(P=0.020).结论·脊髓后角的CCR2可通过增强AMPA和NMDA受体功能来介导BCP大鼠脊髓后角兴奋性突触传递效能的增强,该作用可能是BCP维持的重要机制.
Author 王丽娅
周晔
高坡
AuthorAffiliation 上海交通大学医学院附属国际和平妇幼保健院产科,上海市胚胎源性疾病重点实验室,上海市临床重点专科(建设项目)-"强主体"妇产科,上海 200030%上海交通大学医学院附属仁济医院麻醉科,上海,200127
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ZHOU Ye
GAO Po
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Issue 11
Keywords 趋化因子受体2
脊髓
自发兴奋性突触后电流
骨癌痛
胶状质层
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Title 脊髓趋化因子受体2介导大鼠骨癌痛维持的机制研究
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