P16,P53蛋白及PCNA在癫痫患者海马硬化灶的表达

为了解癫痫病灶胶质增生的机理，对２０例海马硬化灶及１０例对照进行了Ｐ１６、Ｐ５３蛋白及ＰＣＮＡ表达的免疫组化检测。结果：Ｐ１６蛋白在癫痫病灶胶质增生区较对照组表达率降低，差别有统计学意义；Ｐ５３蛋白在癫痫组及对照组均呈阴性反应；ＰＣＮＡ在癫痫灶胶质增生区较对照组胶质细胞表达增强（Ｐ＜０．０１）。上述结果提示，癫痫海马硬化灶胶质增生可能与Ｐ１６蛋白表达减少有关；Ｐ５３蛋白表达在病变区及正常区无明显变化；ＰＣＮＡ参予了胶质细胞增生的调节。

THE EXPRESSION OF P16,P15 PROTEIN AND PCNA IN HIPPOCAMPAL SCLEROSIS FOCI OF EPILEPSY

Epilepsy is a kind of syndrome caused by mutiple factors. Though the pathological changes are different in varied types, gliosis is the common typical change in each type of epilepsy. In order to understand the molecule biological mechanism of gliosis, we tested 20 cases of hippocampal sclerosis focus and 10 controls for their P16 protein(product of tumor suppressor or cyclin dependent kinase inhibitor P16 Ink4 gene), P53 protein(product of tumor suppressor gene p53) and proliferating cell nuclear antigen(PCNA) expression by immunohistochemical method. The result showed:(a) P16 protein expression is mild to medium partially positive in normal temporal hippocampal glial cells, but the expression is markedly decreased or completely negative in hippocampal sclerosis foci( P <0.05); (b) P53 protein expression is negative in glial cells of both normal temporal hippocampal tissue and gliosis focus; (c) PCNA expression is rather low or even completely negative in the glial cells of control group, but mild to medium partially positive in gliosis foci( P <0.05). The upper mentioned results suggest that:(a) the gliosis of epileptic foci may be related to the decreased expression of P16 protein (b) P53 expression is negative in glial cells of normal temporal hippocampal tissue and hippocampal sclerosis foci, which may prove that p53 gene mutation is not likely to be involved in glial cells hyperplasia;(c) although PCNA expression,as an indicator of cell proliferation, is only mild to medium partial positive in hippocampal sclerois foci, the difference between the pathological and normal groups demonstrates increased expression of PCNA in gliosis areas, which further indicates that PCNA participates in glial cells hyperplasia.