崩漏肾虚血瘀证与子宫内膜病理及细胞凋亡调控基因bcl-2、bax关系的研究

Relationship between Kidney Deficiency,Blood Stasis and Endometrial Pathologic Change,Expression of Bcl-2 and Bax in Metrorrhagia and Metrostaxis

为探讨子宫内膜病理改变和细胞凋亡调控基因bcl-2、bax蛋白表达变化与崩漏肾虚血瘀证的关系,采用免疫组化染色测定子宫内膜bcl-2、bax蛋白表达。结果：①肾虚血瘀组、脾虚血瘀组病理分级以单纯性增生为主,肾虚血瘀组以复杂性增生为次,脾虚血瘀组以增生期改变为次,差异显著(P＜0．01)；②bcl-2表达在正常子宫内膜组、脾虚血瘀组、肾虚血瘀组中表达依次递增(P＜0．01)；bax则依次递减(P＜0．01)；bcl-2与bax呈显著负相关(P＜0．01)；③肾虚血瘀组中肾阳虚血瘀、肾阴虚血瘀2组间bcl-2表达差异显著(P＜0．01)。这说明子宫内膜病理改变、bcl-2、bax蛋白表达变化,可以作为崩漏肾虚血瘀证的病理生理基础。

To investigate the relationship between kidney deficiency, blood stasis change, expression of bcl-2 and bax in metrorrhagia and metrostaxis. 30 patients s and endometrial pathologic uffering from metrorrhagia and metrostaxis with kidney deficiency and blood stasis syndrome （group A） were selected, among them there were 15 kidney yin deficiency and blood stasis syndrome （group A1）, 15 kidney yang deficiency and blood stasis syndrome （group A2）. 15 patients with spleen deficiency and blood stasis syndrome （group B）, and 15 normal cases （group C） were selected as control groups. The expressions of bcl-2 and bax were analyzed by immunohistochemistry method. The results showed that ① the simple hyperplasia held dominance both in group A and B, the secondary is complex hyperplasia in group A, and normal proliferative endometrium in group B （P〈0.01）. ② the expressions of bcl-2 increased step by step among group C, B, and A, to the contrary of bax （P〈0.01）, the expression of bcl-2 showed opposite correlation to bax （P〈0.01）. ③ the expressions of bcl-2 had significant difference between group A1 and A2 （P〈0.01）. Conclusion： The endometrial pathologic change, expression of bcl-2 and bax can be used as the pathophysiological basis of kidney deficiency and blood stasis syndrome of metrorrhagia and metrostaxis.