中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2009年
6期
507-509
,共3页
申文%唐元章%刘苏%孙玉娥%张井浪%苏小虎%马正良
申文%唐元章%劉囌%孫玉娥%張井浪%囌小虎%馬正良
신문%당원장%류소%손옥아%장정랑%소소호%마정량
骨肿瘤%疼痛%星形细胞%小神经胶质细胞%脊髓
骨腫瘤%疼痛%星形細胞%小神經膠質細胞%脊髓
골종류%동통%성형세포%소신경효질세포%척수
Bone neoplasms%Pain%Astrocytes%Microglia%Spinal cord
目的 评价脊髓胶质细胞在小鼠骨癌痛形成中的作用.方法 健康雄性C3H/He小鼠40只,周龄8~10周,体重18~22 g,随机分为4组(n=10):假手术组(S组)、骨癌痛组(B组)、PBS组(P组)和米诺环素组(M组).S组跟骨骨髓腔内注射PBS 10 μl;余3组跟骨骨髓腔内注射含2×105个骨纤维肉瘤细胞的PBS 10 μl制备骨癌痛模型,于造模前即刻开始PBS组鞘内注射PBS 5μl,M组鞘内注射米诺环素(用PBS溶解为0.2 mmol/L)5μl,1次/d,连续11 d.于造模前1 d、造模后即刻、3、5、7、9、11 d时测定机械痛阈;于造模后3、7、9、11 d机械痛阈测定结束后测定冷痛阈.痛阈测定结束后处死小鼠,取脊髓组织,测定神经胶质纤维酸性蛋白(GFAP)和CD11b的表达水平.结果 与S组比较,B组和P组造模后3-11 d时、M组造模后3、5 d时机械痛阈升高,B组、P组和M组造模后7~11 d时冷痛阈升高,脊髓CD11b和GFAP表达上调(P<0.05).与B组比较,M组造模后3-11 d时机械痛阈降低,造模后7-11 d时冷痛阈降低,脊髓CD11b和GFAP表达下调(P<0.05).结论 脊髓胶质细胞(星形胶质细胞和小胶质细胞)的激活参与了小鼠骨癌痛的形成.
目的 評價脊髓膠質細胞在小鼠骨癌痛形成中的作用.方法 健康雄性C3H/He小鼠40隻,週齡8~10週,體重18~22 g,隨機分為4組(n=10):假手術組(S組)、骨癌痛組(B組)、PBS組(P組)和米諾環素組(M組).S組跟骨骨髓腔內註射PBS 10 μl;餘3組跟骨骨髓腔內註射含2×105箇骨纖維肉瘤細胞的PBS 10 μl製備骨癌痛模型,于造模前即刻開始PBS組鞘內註射PBS 5μl,M組鞘內註射米諾環素(用PBS溶解為0.2 mmol/L)5μl,1次/d,連續11 d.于造模前1 d、造模後即刻、3、5、7、9、11 d時測定機械痛閾;于造模後3、7、9、11 d機械痛閾測定結束後測定冷痛閾.痛閾測定結束後處死小鼠,取脊髓組織,測定神經膠質纖維痠性蛋白(GFAP)和CD11b的錶達水平.結果 與S組比較,B組和P組造模後3-11 d時、M組造模後3、5 d時機械痛閾升高,B組、P組和M組造模後7~11 d時冷痛閾升高,脊髓CD11b和GFAP錶達上調(P<0.05).與B組比較,M組造模後3-11 d時機械痛閾降低,造模後7-11 d時冷痛閾降低,脊髓CD11b和GFAP錶達下調(P<0.05).結論 脊髓膠質細胞(星形膠質細胞和小膠質細胞)的激活參與瞭小鼠骨癌痛的形成.
목적 평개척수효질세포재소서골암통형성중적작용.방법 건강웅성C3H/He소서40지,주령8~10주,체중18~22 g,수궤분위4조(n=10):가수술조(S조)、골암통조(B조)、PBS조(P조)화미낙배소조(M조).S조근골골수강내주사PBS 10 μl;여3조근골골수강내주사함2×105개골섬유육류세포적PBS 10 μl제비골암통모형,우조모전즉각개시PBS조초내주사PBS 5μl,M조초내주사미낙배소(용PBS용해위0.2 mmol/L)5μl,1차/d,련속11 d.우조모전1 d、조모후즉각、3、5、7、9、11 d시측정궤계통역;우조모후3、7、9、11 d궤계통역측정결속후측정랭통역.통역측정결속후처사소서,취척수조직,측정신경효질섬유산성단백(GFAP)화CD11b적표체수평.결과 여S조비교,B조화P조조모후3-11 d시、M조조모후3、5 d시궤계통역승고,B조、P조화M조조모후7~11 d시랭통역승고,척수CD11b화GFAP표체상조(P<0.05).여B조비교,M조조모후3-11 d시궤계통역강저,조모후7-11 d시랭통역강저,척수CD11b화GFAP표체하조(P<0.05).결론 척수효질세포(성형효질세포화소효질세포)적격활삼여료소서골암통적형성.
Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.