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目的研究乳岩内消霜诱导乳腺癌前病变细胞凋亡的作用,探寻乳岩内消霜治疗乳腺癌前病变的机制。方法 MTT法观察不同浓度乳岩内消霜透皮液对乳腺癌前MCF-10AT细胞的生长抑制作用;流式细胞术检测MCF-10AT细胞凋亡率;Western blotting检测MCF-10AT细胞中bcl-2和bax蛋白;60只雌性未孕SD大鼠,采用二甲基苯并蔥(DMBA)联合雌、孕激素诱导癌前病变模型,同时使用霜剂涂抹大鼠乳房,第10周处死大鼠,进行组织病理学检测;Western blotting分别检测大鼠乳腺组织和MCF-10AT细胞cleaved caspase9、cleaved caspase3蛋白的表达。结果 MTT结果显示,乳岩内消霜透皮液对MCF-10AT细胞增殖有显著抑制作用;1%、2%和4%乳岩内消霜处理MCF-10AT细胞24 h,细胞凋亡率分别为(24.8±4.1)%、(43.2±5.3)%和(65.6±6.8)%;与空白对照组比较,乳岩内消霜和三苯氧胺干预MCF-10AT细胞后bcl-2表达下降,bax表达上升(P<0.05);与正常对照组比较,大鼠乳腺组织和MCF-10AT细胞中乳岩内消霜及三苯氧胺干预组cleaved caspase9、cleaved caspase3表达均明显上升(P<0.01)。结论乳岩内消霜有效抑制乳腺癌前病变发展,可能是通过内源性caspase途径诱导乳腺癌前病变细胞凋亡实现的。
Objective To study the effect of Cream in Cream on apoptosis of breast precancerous lesions and to explore the mechanism of Cream in Cream in the treatment of breast precancerous lesions. Methods MTT assay was used to observe the effect of different concentrations of anti-creosote transdermal fluid on the growth of pre-MCF-10AT cells. Flow cytometry was used to detect the apoptosis rate of MCF-10AT cells. Western blotting was used to detect the expression of bcl-2 And bax protein. Sixty female un-pregnant SD rats were treated with DMBA combined with estrogen and progesterone to induce precancerous lesions. At the same time, The expression of cleaved caspase9 and cleaved caspase3 protein in mammary gland tissue and MCF-10AT cells were detected by Western blotting. Results The results of MTT showed that the creosote cream of creosote significantly inhibited the proliferation of MCF-10AT cells; the apoptosis rate of MCF-10AT cells treated with 1%, 2% and 4% 24.8 ± 4.1%, (43.2 ± 5.3)% and (65.6 ± 6.8)%, respectively. Compared with the blank control group, the bcl-2 expression and the bax expression were increased in MCF-10AT cells treated with defatted cream and tamoxifen (P < 0.05). Compared with the normal control group, the expressions of cleaved caspase9 and cleaved caspase3 in mammary gland and MCF-10AT cells were significantly increased (P <0.01). Conclusion YURU can effectively inhibit the development of breast precancerous lesions, which may be induced by endogenous caspase pathway to induce apoptosis of breast precancerous lesions.