目的：研究内异方对子宫内膜异位症（EMs）模型大鼠异位内膜组织中NF-kB、Caspase -3、Bcl-2、 Bax、HIF-1α的表达水平，探讨内异方对EMs大鼠异位内膜细胞增殖与凋亡的作用。方法：手术复制模型后结合人工干预刺激建立瘀毒证模型。造模成功后随机分为模型组、常氧内异方低剂量组、常氧内异方高剂量组、缺氧内异方低剂量组、缺氧内异方高剂量组、散结镇痛胶囊组。各组大鼠连续灌胃4周后，对比观察用药过程中各组大鼠的行为学表现；取异位组织采用HE染色及蛋白印迹技术检测EMs大鼠在位内膜、异位内膜中的NF-kB、Caspase -3、Bcl-2、 Bax、HIF-1α的表达及病理形态学观察。结果：1.内异方能减少异位病灶的血供、减少腺体形成、降低炎细胞浸润等来缩小异位病灶，改善盆腔粘连。2.与模型组相比，常中高组大鼠异位内膜中Hif-1α降低，差别有统计学意义（P<0.05）。3.与模型组相比，常中低组、散结镇痛胶囊组Ems大鼠Hif-1α降低，差别有统计学意义（P<0.05）, 常中高组显著降低（P<0.01）；4.与模型组相比，其他各组Ems大鼠异位内膜中Caspase -3 、Bax/Bcl-2水平均升高，差别有统计学意义（P<0.05）。结论:内异方可能通过下调NF-kB、HIF-1α、增强Caspase-3、Bax/Bcl-2表达，促进异位细胞凋亡来阻断异位内膜的增殖，缩小异位病灶。
objective: to study the expression levels of nf-kb, caspase-3, bcl-2, Bax, and hif-1 alpha in endometriosis (EMs) rat endometrium tissues and investigate the effect of endometriosis on the proliferation and apoptosis of EMs rat endometriosis cells. Methods: the model of stasis and toxin syndrome was established after surgical duplication combined with artificial intervention. After the successful modeling, the patients were randomly divided into the model group, the low-dose normoxic heterofrequency prescription group, the high-dose normoxic heterofrequency prescription group, the low-dose hypoxic heterofrequency prescription group, the high-dose hypoxic heterofrequency prescription group, and the sanjie analgesic capsule group. After continuous gavage for 4 weeks, the behavioral manifestations of rats in each group were compared and observed. The expression of nf-kb, caspase-3, bcl-2, Bax and hif-1 alpha in the endometrium and ectopic endometrium of EMs rats were detected by HE staining and western blot. Results: 1. Internal heterotopia can reduce the blood supply of the heterotopic lesion, reduce the formation of glands, reduce the infiltration of inflammatory cells and so on to reduce the heterotopic lesion and improve pelvic adhesion. 2. Compared with the model group, hif-1 alpha was decreased in the ectopic endometrium of rats in the normal, medium and high groups, and the difference was statistically significant (P<0.05). 3. Compared with the model group, hif-1 alpha was decreased in Ems rats in the chang zhong low group and SAN jie zhen tong capsule group, with statistically significant difference (P<0.05), and significantly decreased in the chang zhong high group (P<0.01). 4. Compared with the model group, the levels of caspase-3 and Bax/ bcl-2 in the ectoplasmic intima of Ems rats in other groups were increased, with statistically significant differences (P<0.05). Conclusion: endometriosis may inhibit the proliferation of endometriosis by down-regulating the expression of nf-kb, hif-1 alpha, enhancing the expression of caspase-3 and Bax/ bcl-2, promoting the apoptosis of ectopic cells, and reducing the ectopic lesions.