CAJ | 학술논문

目的：研究蒙药乳腺-I（M-I）号对乳腺增生大鼠乳腺组织细胞增殖和凋亡的影响。方法实验动物采用雌性未孕Wistar大鼠，乳腺增生模型复制方法为大鼠肌肉注射苯甲酸雌二醇0.5 mg/（kg·d）25 d，随后肌肉注射黄体酮4 mg/（kg·d）5 d。实验共分为6组：正常对照组、模型对照组，均给与生理盐水灌胃；阳性药对照组，给与三苯氧胺1.8 mg/kg灌胃；M-I号低、中和高剂量组分别给予M-I号0.5 g/kg、1.0 g/kg和3.0 g/kg灌胃。给药结束后，通过对各组大鼠乳腺组织进行HE染色，观察大鼠乳腺组织增生的程度，应用免疫组织化学方法观察乳腺组织中增殖细胞核抗原、细胞凋亡相关调控因子Bcl-2、Bax的表达。结果 M-I号能够抑制乳腺组织增生，降低PCNA和Bcl-2的表达活性（P<0.05），增加Bax的表达活性（P<0.05），进而抑制乳腺组织细胞增殖，促进细胞凋亡（P<0.05）。结论 M-I号对乳腺增生大鼠有较好的治疗作用，其治疗机制与抑制大鼠乳腺组织细胞增殖，促进细胞凋亡的作用有关。
목적：연구몽약유선-I（M-I）호대유선증생대서유선조직세포증식화조망적영향。방법실험동물채용자성미잉Wistar대서，유선증생모형복제방법위대서기육주사분갑산자이순0.5 mg/（kg·d）25 d，수후기육주사황체동4 mg/（kg·d）5 d。실험공분위6조：정상대조조、모형대조조，균급여생리염수관위；양성약대조조，급여삼분양알1.8 mg/kg관위；M-I호저、중화고제량조분별급여M-I호0.5 g/kg、1.0 g/kg화3.0 g/kg관위。급약결속후，통과대각조대서유선조직진행HE염색，관찰대서유선조직증생적정도，응용면역조직화학방법관찰유선조직중증식세포핵항원、세포조망상관조공인자Bcl-2、Bax적표체。결과 M-I호능구억제유선조직증생，강저PCNA화Bcl-2적표체활성（P<0.05），증가Bax적표체활성（P<0.05），진이억제유선조직세포증식，촉진세포조망（P<0.05）。결론 M-I호대유선증생대서유교호적치료작용，기치료궤제여억제대서유선조직세포증식，촉진세포조망적작용유관。
Objective To observe effects of Mongolian Remedy RuXian-I on proliferation and apoptosis of Mammary Gland Hyperplastic Tissue in Rats. Method 8 rats randomly chosen from Forty-eight virgin female Wistar rats were regarded as normal. The others were injected intramuscular with E 2(0.5 mg/kg) per day for 25 d and P(4 mg/kg) per day for 5 d. The rats in normal control group were injected with normal saline. Then disease model group was randomly divided into 5 groups:model control group, positive control group, M-I low dosage group, M-I middle dosage group and M-I high dosage group. The rats in different groups were respectively treated with normal saline, tamoxifen, M-I 0.5, 1.0 and 3.0 g/kg for 28 d. Then the pathological changes and expressions of Bax, Bcl-2, PCNA in breast tissues were measured. Results Compared with normal control group, expression of PCNA and Bcl-2 in model control group were obviously higher(P<0.01, P<0.05), while the expression of Bax were obviously lower (P<0.01). Compared with model control group, the expressions of PCNA and Bcl-2 in breast tissue in M-I high dosage group were obviously lower, while the expressions of Bax breast tissues were obviously higher(P<0.05). Conclusion Treatment mechanism of M-I may be related with inhibited cell proliferation and promote cell apoptosis in the breast tissue.