摘要
目的对比研究丝裂素激活蛋白激酶(MAPKs)在增生与正常前列腺组织中的表达,探讨良性前列腺增生发病的分子生物学机制。方法采用W estern B lot及免疫组织化学方法,检测增生及正常前列腺组织中ERK、JNK和p38MAPK的表达情况。结果与正常前列腺组织相比,增生组织ERK的平均灰度值(wh ite^b lack,0~255)和阳性细胞百分率明显升高,JNK和p38MAPK的检测结果则与之相反。ERK染色主要位于细胞核和细胞质内,在增生组织上皮细胞及基质细胞的染色阳性率均高于正常前列腺组织。结论ERK在良性前列腺增生组织中过表达,从而导致细胞增生指数增加,JNK和p38MAPK低表达导致凋亡减少,促进疾病的发生和发展。
Objective To investigate the expression of mitogen-activated protein kinases （MAPKs） in benign prostatic hyperplasia（BPH） and normal prostatic tissue and explore the molecular biology mechanism of pathogenesis of BPH. Methods To detect the expression of extracellular signal-regulated kinase（ERK） ,c-Jun N-terminal kinase （JNK） and p38MAPK in 64 cases of BPH and 16 cases of normal prostates with western blot analysis and immunohistochemical techniques. Results The average gray value of ERK and percentage of ERK positive cells were higher in BPH compared with normal prostates, but the average gray values of JNK and p38 in BPH were lower than that in normal prostate（ P 〈0.01 ）. The immunostaining product of ERK was mainly located in nuclei and cytoplasm,and the positive staining rates of epithelial cells and stromal cells in BPH were higher than that in normal prostate prominantly. Conclusion The overexpression of ERK leading to the increase of proliferative index of cells and downexpressions of JNK and p38MAPK leading to the decrease of apoptosis maybe involved in the development of BPH.
出处
《解剖科学进展》
CAS
2005年第3期203-205,i0004,共4页
Progress of Anatomical Sciences
基金
辽宁省科委重大新产品基金(C991147)
关键词
MAPK
信号传导
良性前列腺增生
发病机制
MAPK
signal transduction
benign prostatic hyperplasis （BPH）
pathogenesis
