中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
9期
1092-1094
,共3页
金迪%杨建平%胡计嬅%王丽娜%侯永恒
金迪%楊建平%鬍計嬅%王麗娜%侯永恆
금적%양건평%호계화%왕려나%후영항
骨肿瘤%疼痛%1-磷脂酰肌醇3-激酶%蛋白质丝氨酸苏氨酸激酶%小神经胶质细胞%脊髓
骨腫瘤%疼痛%1-燐脂酰肌醇3-激酶%蛋白質絲氨痠囌氨痠激酶%小神經膠質細胞%脊髓
골종류%동통%1-린지선기순3-격매%단백질사안산소안산격매%소신경효질세포%척수
Bone neoplasms%Pain%1-Phosphatidylinositol 3-kinase%Protein-serine-threonine kinases%Nicroglia%Spinal cord
目的 评价脊髓磷脂酰肌醇-3-激酶/丝氨酸-苏氨酸蛋白激酶(PDK/Akt)信号通路在大鼠骨癌痛维持中的作用及其与小胶质细胞活化的关系.方法 健康雌性SD大鼠40只,体重180 ～200 g,采用随机数字表法将其分为5组(n=8):假手术组(S组)、PI3K抑制剂LY294002组(L组)、骨癌痛组(BCP组)、骨癌痛+二甲基亚砜组(BCP+D组)、骨癌痛+LY294002组(BCP+L组).采用左侧胫骨干骺端骨髓腔内接种Walker256乳腺癌细胞的方法制备大鼠骨癌痛模型.于接种后7-9 d,L组和BCP+L组鞘内注射LY294002 2.5 μg/10μL,S组和BCP组鞘内注射生理盐水10μl,BCP+D组鞘内注射5％ DMSO 10μL,1次/d.于接种前1d及接种后1、3、5、7、8、9d给药后测定机械痛阈.于接种后9d行为学测试结束后处死大鼠取L4-6脊髓组织,采用免疫荧光染色法检测脊髓背角小胶质细胞的活化水平.结果 与S组比较,BCP组、BCP+D组和BCP+L组机械痛阈降低,脊髓背角小胶质细胞活化水平升高(P＜0.01).与BCP组和BCP+D组比较,BCP+L组机械痛阈升高,脊髓背角小胶质细胞活化水平降低(P＜0.05).结论 脊髓PI3K/Akt信号通路可能通过活化背角小胶质细胞参与大鼠骨癌痛的维持.
目的 評價脊髓燐脂酰肌醇-3-激酶/絲氨痠-囌氨痠蛋白激酶(PDK/Akt)信號通路在大鼠骨癌痛維持中的作用及其與小膠質細胞活化的關繫.方法 健康雌性SD大鼠40隻,體重180 ～200 g,採用隨機數字錶法將其分為5組(n=8):假手術組(S組)、PI3K抑製劑LY294002組(L組)、骨癌痛組(BCP組)、骨癌痛+二甲基亞砜組(BCP+D組)、骨癌痛+LY294002組(BCP+L組).採用左側脛骨榦骺耑骨髓腔內接種Walker256乳腺癌細胞的方法製備大鼠骨癌痛模型.于接種後7-9 d,L組和BCP+L組鞘內註射LY294002 2.5 μg/10μL,S組和BCP組鞘內註射生理鹽水10μl,BCP+D組鞘內註射5％ DMSO 10μL,1次/d.于接種前1d及接種後1、3、5、7、8、9d給藥後測定機械痛閾.于接種後9d行為學測試結束後處死大鼠取L4-6脊髓組織,採用免疫熒光染色法檢測脊髓揹角小膠質細胞的活化水平.結果 與S組比較,BCP組、BCP+D組和BCP+L組機械痛閾降低,脊髓揹角小膠質細胞活化水平升高(P＜0.01).與BCP組和BCP+D組比較,BCP+L組機械痛閾升高,脊髓揹角小膠質細胞活化水平降低(P＜0.05).結論 脊髓PI3K/Akt信號通路可能通過活化揹角小膠質細胞參與大鼠骨癌痛的維持.
목적 평개척수린지선기순-3-격매/사안산-소안산단백격매(PDK/Akt)신호통로재대서골암통유지중적작용급기여소효질세포활화적관계.방법 건강자성SD대서40지,체중180 ～200 g,채용수궤수자표법장기분위5조(n=8):가수술조(S조)、PI3K억제제LY294002조(L조)、골암통조(BCP조)、골암통+이갑기아풍조(BCP+D조)、골암통+LY294002조(BCP+L조).채용좌측경골간후단골수강내접충Walker256유선암세포적방법제비대서골암통모형.우접충후7-9 d,L조화BCP+L조초내주사LY294002 2.5 μg/10μL,S조화BCP조초내주사생리염수10μl,BCP+D조초내주사5％ DMSO 10μL,1차/d.우접충전1d급접충후1、3、5、7、8、9d급약후측정궤계통역.우접충후9d행위학측시결속후처사대서취L4-6척수조직,채용면역형광염색법검측척수배각소효질세포적활화수평.결과 여S조비교,BCP조、BCP+D조화BCP+L조궤계통역강저,척수배각소효질세포활화수평승고(P＜0.01).여BCP조화BCP+D조비교,BCP+L조궤계통역승고,척수배각소효질세포활화수평강저(P＜0.05).결론 척수PI3K/Akt신호통로가능통과활화배각소효질세포삼여대서골암통적유지.
Objective To evaluate the role of spinal phosphatidyl-inositol 3-kinase/Akt (PI3k/Akt) signaling pathway in the maintenance of bone cancer pain (BCP) in rats and its relationship with microglial activation.Methods Forty healthy female Sprague-Dawley rats,weighing 180-200 g,were randomly divided into 5 groups (n =8 each):sham operation group (group S) ; PI3K inhibitor LY294002 group (group L) ; group BCP; BCP + dimethyl sulfoxide (DMSO) group (group BCP + D) ; BCP + LY294002 group (group BCP + L).BCP was induced by inoculating Walker 256 mammary gland carcinoma cells into the medullary cavity of the left tibia.At 7-9 days after inoculation,LY294002 2.5 μg/10 μl was injected intrathecally in L and BCP + L groups,normal saline 10 μl was injected intrathecally in S and BCP groups,and 5％ DMSO 10 μl was injected intrathecally in BCP+ D group once a day.Mechanical paw withdrawal threshold (MWT) was measured at 1 day before inoculation and 1,3,5,7,8 and 9 days after inoculation.The rats were sacrificed after MWT was measured on day 9 after inoculation and the L4-6 segments of the spinal cord were removed to determinate the activation of spinal microglia using immunofluorescence.Results Compared with group S,MWT was significantly decreased,and the activation of spinal microglia was increased in BCP,BCP + D and BCP+ L groups.Compared with BCP and BCP + D groups,MWT was significantly increased,and the activation of spinal microglia was decreased in BCP + D group.Conclusion Spinal PI3K/Akt signaling pathway is involved in the maintenance of BCP possibly through activating microglia in spinal dorsal horns of rats.
