中国疼痛医学杂志
中國疼痛醫學雜誌
중국동통의학잡지
CHINESE JOURNAL OF PAIN MEDICINE
2010年
2期
96-99
,共4页
高宇%郑婧%杨小龙%李勇光%梅敦成%杨庆红%王云霞
高宇%鄭婧%楊小龍%李勇光%梅敦成%楊慶紅%王雲霞
고우%정청%양소룡%리용광%매돈성%양경홍%왕운하
维生素B_6%神经病理性疼痛%磷酸化细胞外信号调节激酶
維生素B_6%神經病理性疼痛%燐痠化細胞外信號調節激酶
유생소B_6%신경병이성동통%린산화세포외신호조절격매
Vitamine B6%Neuropathic pain%p-ERK
目的:观察维生素B_6(VitB_6)对神经病理性疼痛大鼠机械痛敏、热痛敏及L4~L5背根神经节(DRG)磷酸化细胞外信号调节激酶(P-ERK)表达的影响.方法:选择6只正常SD大鼠作为对照组(control),另选择鞘内置管3天后无神经损伤症状的SD雄性大鼠54只,随机分为3组(n=18):假手术组(sham):只分离坐骨神经;CCI组:结扎坐骨神经;CCI+Vit B6组:坐骨神经结扎后鞘内注射VitB_610mg/kg/d,连续两周.各组术前2天和术后1、3、5、7、10、14天测定各组大鼠热缩足反射潜伏期(TWL)、机械缩足反射阈值(MWT).除control组外其余各组分别在术后3d、7d和14d处死大鼠,采用免疫组织化学法观察L4~5 DRG和p-ERK的表达.结果:与sham组比较,CCI组术后各天TWL、MWT明显降低(P<0.01);与CCI组比较,CCI+VitB_6组术后3、5、7、10、14天TWL明显增高(3天P<0.05,5、7、10、14天P<0.01),而术后各天MWT无明显差别.术后3、7、14天,CCI组结扎侧L4,5背根节p-ERK阳性细胞率明显高于sham组(P<0.01),CCI+Vit B_6组结扎侧L4,5背根节p-ERK阳性细胞率明显低于CCI组(P<0.01).结论:背根神经节ERK活化参与神经病理性疼痛信号传递,鞘内注射Vit B_6抑制CCI大鼠热痛敏,其机制可能包括通过上游机制抑制ERK激活.
目的:觀察維生素B_6(VitB_6)對神經病理性疼痛大鼠機械痛敏、熱痛敏及L4~L5揹根神經節(DRG)燐痠化細胞外信號調節激酶(P-ERK)錶達的影響.方法:選擇6隻正常SD大鼠作為對照組(control),另選擇鞘內置管3天後無神經損傷癥狀的SD雄性大鼠54隻,隨機分為3組(n=18):假手術組(sham):隻分離坐骨神經;CCI組:結扎坐骨神經;CCI+Vit B6組:坐骨神經結扎後鞘內註射VitB_610mg/kg/d,連續兩週.各組術前2天和術後1、3、5、7、10、14天測定各組大鼠熱縮足反射潛伏期(TWL)、機械縮足反射閾值(MWT).除control組外其餘各組分彆在術後3d、7d和14d處死大鼠,採用免疫組織化學法觀察L4~5 DRG和p-ERK的錶達.結果:與sham組比較,CCI組術後各天TWL、MWT明顯降低(P<0.01);與CCI組比較,CCI+VitB_6組術後3、5、7、10、14天TWL明顯增高(3天P<0.05,5、7、10、14天P<0.01),而術後各天MWT無明顯差彆.術後3、7、14天,CCI組結扎側L4,5揹根節p-ERK暘性細胞率明顯高于sham組(P<0.01),CCI+Vit B_6組結扎側L4,5揹根節p-ERK暘性細胞率明顯低于CCI組(P<0.01).結論:揹根神經節ERK活化參與神經病理性疼痛信號傳遞,鞘內註射Vit B_6抑製CCI大鼠熱痛敏,其機製可能包括通過上遊機製抑製ERK激活.
목적:관찰유생소B_6(VitB_6)대신경병이성동통대서궤계통민、열통민급L4~L5배근신경절(DRG)린산화세포외신호조절격매(P-ERK)표체적영향.방법:선택6지정상SD대서작위대조조(control),령선택초내치관3천후무신경손상증상적SD웅성대서54지,수궤분위3조(n=18):가수술조(sham):지분리좌골신경;CCI조:결찰좌골신경;CCI+Vit B6조:좌골신경결찰후초내주사VitB_610mg/kg/d,련속량주.각조술전2천화술후1、3、5、7、10、14천측정각조대서열축족반사잠복기(TWL)、궤계축족반사역치(MWT).제control조외기여각조분별재술후3d、7d화14d처사대서,채용면역조직화학법관찰L4~5 DRG화p-ERK적표체.결과:여sham조비교,CCI조술후각천TWL、MWT명현강저(P<0.01);여CCI조비교,CCI+VitB_6조술후3、5、7、10、14천TWL명현증고(3천P<0.05,5、7、10、14천P<0.01),이술후각천MWT무명현차별.술후3、7、14천,CCI조결찰측L4,5배근절p-ERK양성세포솔명현고우sham조(P<0.01),CCI+Vit B_6조결찰측L4,5배근절p-ERK양성세포솔명현저우CCI조(P<0.01).결론:배근신경절ERK활화삼여신경병이성동통신호전체,초내주사Vit B_6억제CCI대서열통민,기궤제가능포괄통과상유궤제억제ERK격활.
Objective:To investigate the effect of vitamine B_6 (Vit B_6) on neuropathic pain and the expression of p-ERK in L4,5 DRG in CCI rats.Methods:6 SD rats were used as control group without any operation,another 54 male SD rats,which showed no signs of never injury 3 days after IT catheterization with the tip of catheter reaching the lumbar region,were randomly divided into 3 groups ( n = 18 ): Sham,CCI and CCI + Vit B_6 group.CCI + Vit B_6 group was treated with intrathecal injection Vit B_6 for two weeks.Thermal withdrawal latency(TWL) and mechanical withdrawal threshold(MWT) of the rats were measured on 1,2 pre-operative and 1,3,5,7,10,14 post-operative days.The expression of p-ERK of ipsilateral L4,5 DRG were assessed by immunohistochemistry on 3,7,14 post-operative days.Results:TWL and MWT in CCI group were significantly lower than sham group on every post-operative day (P <0.01 );TWL in CCI + Vit B_6 group was higher than CCI group on 3,5,7,10,14 post-operative days(P <0.05 on 3 postoperative day,P < 0.01 on 5,7,10,14 postoperative days),there was no significant difference in MWT between the two groups.The increase of the percentage of immunoreactive p-ERK neurons in the ipsilateral L4,5 DRG in CCI group was evident at 3,7,14d after surgery compared with those of the sham group ( P <0.01 ).The intrathecal injection of Vit B_6 markedly suppressed the increase of CCI induced p-ERK expression.Conclusion:ERK activation in dorsal root ganglion may contribute to the transmission of neuropathic pain,Vit B_6 can alleviate thermal hyperalgesia induced by CCI,the mechanism may include inhibiting ERK activation from its upper stream.