国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
International Journal of Anesthesiology and Resuscitation
2015年
10期
884-887
,共4页
范后宝%张婷%孙凯%申文
範後寶%張婷%孫凱%申文
범후보%장정%손개%신문
骨癌痛%脊髓%碱性成纤维细胞生长因子-2%磷酸化c-Jun氨基末端激酶
骨癌痛%脊髓%堿性成纖維細胞生長因子-2%燐痠化c-Jun氨基末耑激酶
골암통%척수%감성성섬유세포생장인자-2%린산화c-Jun안기말단격매
Bone cancer pain%Spinal cord%Fibroblast growth factor basic-2%Phospho-c-Jun N-terminal kinase
目的 研究碱性成纤维细胞生长因子-2/c-Jun氨基末端激酶(fibroblast growth factor basic-2/c-Jun N-terminalkinase, FGF-2/JNK)通路在大鼠骨癌痛(bone cancer pain,BCP)中的作用. 方法 雌性SD大鼠32只,体重180 g～200 g,采用随机数字表法分为4组,每组8只:假手术组(S组)、BCP组(B组)、BCP+磷酸盐缓冲液(phosphate buffered saline,PBS)组(BP组)、BCP+FGF-2中和抗体组(BA组).B组在大鼠胫骨平台注入Walker 256乳腺癌细胞5μl(4×105个/ml),S组注入等量的生理盐水,术后10、11、12d,BA组鞘内注射FGF2中和抗体(10 μg/10μ1),BP组鞘内注射等量的PBS.分别于注射肿瘤细胞前1 d(T0)及注射肿瘤细胞后3、5、7、10、12、14 d(T1～T6)测定大鼠的机械缩足反射阈值(paw withdrawal mechanical threshold,PWMT);术后14d处死大鼠,取脊髓腰膨大,采用Western blot检测脊髓磷酸化JNK(phospho-JNK,p4NK)的表达.结果 与S组比较,B组R～T6时[(9.4±1.4)、(7.9±1.4)、(6.0±1.5)、(2.8±1.2)、(2.5±1.3)g]、BP组T2～T6时[(9.4±1.4)、(6.9±1.7)、(5.4±1.7)、(2.5±0.9)、(2.3±0.8)g]、BA组T2～T4时[(10.3±1.9)、(7.7±1.3)、(4.8±11)g]大鼠PWMT均明显下降(P＜0.05);与B组和BP组比较,T5-6时,BA组大鼠PWMT明显升高(P＜0.05),分别为T5(9.0±1.0)g、T6(9.6±1.2)g.与S组比较,B组和BP组p-JNK的表达量明显升高(P＜0.05),分别为(2.17±0.08)、(1.89±0.07)g;与B组比较,BA组pqNK的表达量(1.12±0.03)g明显降低(P＜0.05).结论 脊髓FGF-2/JNK通路参与了大鼠BCP的调控.
目的 研究堿性成纖維細胞生長因子-2/c-Jun氨基末耑激酶(fibroblast growth factor basic-2/c-Jun N-terminalkinase, FGF-2/JNK)通路在大鼠骨癌痛(bone cancer pain,BCP)中的作用. 方法 雌性SD大鼠32隻,體重180 g～200 g,採用隨機數字錶法分為4組,每組8隻:假手術組(S組)、BCP組(B組)、BCP+燐痠鹽緩遲液(phosphate buffered saline,PBS)組(BP組)、BCP+FGF-2中和抗體組(BA組).B組在大鼠脛骨平檯註入Walker 256乳腺癌細胞5μl(4×105箇/ml),S組註入等量的生理鹽水,術後10、11、12d,BA組鞘內註射FGF2中和抗體(10 μg/10μ1),BP組鞘內註射等量的PBS.分彆于註射腫瘤細胞前1 d(T0)及註射腫瘤細胞後3、5、7、10、12、14 d(T1～T6)測定大鼠的機械縮足反射閾值(paw withdrawal mechanical threshold,PWMT);術後14d處死大鼠,取脊髓腰膨大,採用Western blot檢測脊髓燐痠化JNK(phospho-JNK,p4NK)的錶達.結果 與S組比較,B組R～T6時[(9.4±1.4)、(7.9±1.4)、(6.0±1.5)、(2.8±1.2)、(2.5±1.3)g]、BP組T2～T6時[(9.4±1.4)、(6.9±1.7)、(5.4±1.7)、(2.5±0.9)、(2.3±0.8)g]、BA組T2～T4時[(10.3±1.9)、(7.7±1.3)、(4.8±11)g]大鼠PWMT均明顯下降(P＜0.05);與B組和BP組比較,T5-6時,BA組大鼠PWMT明顯升高(P＜0.05),分彆為T5(9.0±1.0)g、T6(9.6±1.2)g.與S組比較,B組和BP組p-JNK的錶達量明顯升高(P＜0.05),分彆為(2.17±0.08)、(1.89±0.07)g;與B組比較,BA組pqNK的錶達量(1.12±0.03)g明顯降低(P＜0.05).結論 脊髓FGF-2/JNK通路參與瞭大鼠BCP的調控.
목적 연구감성성섬유세포생장인자-2/c-Jun안기말단격매(fibroblast growth factor basic-2/c-Jun N-terminalkinase, FGF-2/JNK)통로재대서골암통(bone cancer pain,BCP)중적작용. 방법 자성SD대서32지,체중180 g～200 g,채용수궤수자표법분위4조,매조8지:가수술조(S조)、BCP조(B조)、BCP+린산염완충액(phosphate buffered saline,PBS)조(BP조)、BCP+FGF-2중화항체조(BA조).B조재대서경골평태주입Walker 256유선암세포5μl(4×105개/ml),S조주입등량적생리염수,술후10、11、12d,BA조초내주사FGF2중화항체(10 μg/10μ1),BP조초내주사등량적PBS.분별우주사종류세포전1 d(T0)급주사종류세포후3、5、7、10、12、14 d(T1～T6)측정대서적궤계축족반사역치(paw withdrawal mechanical threshold,PWMT);술후14d처사대서,취척수요팽대,채용Western blot검측척수린산화JNK(phospho-JNK,p4NK)적표체.결과 여S조비교,B조R～T6시[(9.4±1.4)、(7.9±1.4)、(6.0±1.5)、(2.8±1.2)、(2.5±1.3)g]、BP조T2～T6시[(9.4±1.4)、(6.9±1.7)、(5.4±1.7)、(2.5±0.9)、(2.3±0.8)g]、BA조T2～T4시[(10.3±1.9)、(7.7±1.3)、(4.8±11)g]대서PWMT균명현하강(P＜0.05);여B조화BP조비교,T5-6시,BA조대서PWMT명현승고(P＜0.05),분별위T5(9.0±1.0)g、T6(9.6±1.2)g.여S조비교,B조화BP조p-JNK적표체량명현승고(P＜0.05),분별위(2.17±0.08)、(1.89±0.07)g;여B조비교,BA조pqNK적표체량(1.12±0.03)g명현강저(P＜0.05).결론 척수FGF-2/JNK통로삼여료대서BCP적조공.
Objective To evaluate the role of fibroblast growth factor basic-2/c-Jun N-terminal kinase(FGF-2/JNK) pathway in rats with bone cancer pain(BCP).Methods Thirty two female SD rats were randomly divided into sham group(group S, n=8), BCP group(group B, n=8), BCP+PBS group(group BP, n=8), BCP+FGF-2 neutralizing antibody group(group BA, n=8).The rat models of bone cancer pain were developed by intra-tibia inoculation of Walker 256 mammary gland cells.The rats of sham group were inoculated by saline without any cells.1 d before inoculation (T0) and on 3, 5, 7, 10, 12 and 14 d (T1-T6) after inoculation, the paw withdrawal mechanical threshold (PWMT) of mechanical stimulus with von-Frey filaments was measured.On 10, 11, 12 d, the rats of group BP and group BA were intrathecal injected with drugs respectively.The rats were then sacrificed and L4-5 segments of the spinal cord were removed for determination of p-JNK expression in spinal cord using Western blot.Results Compared with group S, a significant decrease of PWMT was observed on T2-T6 in group B and group BP (P＜0.05), the PMWT in group B on T2-T6 was[(9.4±1.4), (7.9±1.4), (6.0±1.5), (2.8±1.2), (2.5±1.3)g], in group BP[(9.4±1.4), (6.9±1.7), (5.4±1.7), (2.5±0.9), (2.3±0.8) g], and on T2-T4 [(10.3±1.90), (7.7±1.3), (4.8±1.1) g] in group BA(P＜0.05), respectively.Compared with group B, the PWMT on T5 and T6 [(9.0±1.0), (9.6±1.2) g] were significantly decreased in group BA(P＜0.05).Compared with group S, the expression of p-JNK was upregulated both in group B and group BP(P＜0.01).Compared with group B [(2.17±0.08) g], a significant decrease of the expression of p-JNK was observed in group BA [(1.12±0.03) g](P＜0.05).Conclusions FGF-2/JNK pathway is involved in the mechanism of BCP in rats.
