摘要
目的:研究腺性膀胱炎病变中促分裂原活化蛋白激酶(MAPK)p42/44和p38的含量水平,探讨其可能的发生机制。方法:应用Westernblot法检测腺性膀胱炎、膀胱普通炎症、膀胱移行细胞癌和正常膀胱组织中p42/44和p38MAPK的含量,并进行比较分析。结果:腺性膀胱炎与膀胱癌组织中p42/44的水平显著高于正常膀胱组织(P<0.01),膀胱普通炎性组织p42/44蛋白水平只轻度增高,但其组织p38水平最高(P<0.01)。膀胱癌组织的p38最低,与腺性膀胱炎比较有显著性差异(P<0.05),与正常膀胱组织比较无差异。结论:腺性膀胱炎的p42/44和p38MAPK信号传导通路不同的激活或抑制可能是细胞增殖、转化和恶性变的重要机制。
Objective：To detect the levels of p42/44 and p38 mitogen-activated protein kinase （MAPK） in cystitis glandularis,and to explore the possible pathogenesis of cystitis glandularis. Methods：The levels of p42/44 and p38 MAPK in tissues sampled from patients with cystitis glandularis, ordinary cystitis, and transitional cell carcinoma of bladder and in normal bladder tissues were detected with Westem blot. Results：The level of p42/44 MAPK in cystitis glandularis and tmnsitional cell carcinoma of bladder were significantly higher than that in normal bladder tissues （P 〈 0.01 ）. The level of p42/44 MAPK slightly increased in ordinary cystitis,and no significant difference in the level of p42/44 MAPK was found between ordinary cystitis and normal bladder tissues. The level of p38 MAPK was the highest in ordinary cystitis and lowest in transitional cell carcinoma of bladder, and no difference in the level of p38 MAPK was found between transitional cell carcinoma of bladder and normal bladder tissue. Conclusion：The activation and inhibition of p42/44 or p38 signal transduction pathway,which may be one of the important mechanisms in the proliferation, differentiation, and carcinogenesis in cystitis glandularis, are different from those in ordinary cystitis and transitional cell carcinoma of bladder.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2007年第1期71-72,共2页
Journal of China Medical University
基金
辽宁省教育厅高校科研基金资助项目(20122174)
关键词
腺性膀胱炎
移行细胞癌
促分裂原活化蛋白激酶
cystitis glandularis
tmnsitional cell carcinoma
mitogen-activated protein kinase
