目的 研究积雪草酸（AA）对前列腺癌PC-3细胞作用及分子机制。方法 采用CCK8法检测积雪草酸（5、10、20、40、80、160μmol·L^-1）对PC-3细胞活力的影响；采用Hochest法和Annexin V/PI法检测积雪草酸（20、30、40μmol·L^-1）对PC-3细胞凋亡的影响；采用JC-1法检测积雪草酸对PC-3细胞线粒体膜电位的影响；采用Western blotting法检测积雪草酸对PC-3细胞线粒体凋亡途径和Janus激酶2（JAK2）/信号转导与转录活化因子3（STAT3）信号通路相关蛋白表达水平的影响。采用Annexin V/PI法、JC-1法、Western blotting法检测JAK2激动剂coumermycin A1（C-A1）对积雪草酸诱导PC-3细胞线粒体凋亡及相关蛋白表达的影响。结果 与对照组比较，积雪草酸可浓度及时间相关性地抑制PC-3细胞增殖，20～160μmol·L^-1组差异显著（P＜0.01），作用24、48、72h后的半数抑制浓度（IC₅₀）值分别为29.98、23.04、13.81μmol·L^-1；20、30、40μmol·L^-1积雪草酸显著促进PC-3细胞凋亡（P＜0.05、0.01）；可明显导致PC-3细胞线粒体膜电位下降；显著上调PC-3细胞线粒体凋亡相关Bax、cleaved Caspase-3的蛋白表达（P＜0.05、0.01），显著下调Bcl-2的蛋白表达（P＜0.05、0.01），显著抑制JAK2/STAT3信号通路JAK2和STAT3的磷酸化水平（P＜0.05、0.01）。与积雪草酸组比较，积雪草酸＋C-A1显著抑制PC-3细胞的凋亡水平（P＜0.01），明显抑制PC-3细胞线粒体膜电位下降，显著下调Bax、cleaved Caspase-3蛋白表达（P＜0.01），显著上调Bcl-2蛋白表达（P＜0.01），显著提升JAK2和STAT3的磷酸化水平（P＜0.01）。结论 积雪草酸可通过抑制JAK2/STAT3信号通路诱导前列腺癌细胞发生线粒体凋亡，进而发挥抗前列腺癌作用。

Objective To study the effects and molecular mechanism of asiatic acid (AA) on prostate cancer PC-3 cells. Method CCK8 assay was used to detect the effect of AA (5, 10, 20, 40, 80, and 160 μmol·L^-1) on PC-3 cell proliferation. Hochest assay and Annexin V/PI assay were used to detect the effect of AA (20, 30, and 40 μmol·L^-1) on PC-3 cell apoptosis. JC-1 method was used to detect the effect of AA on mitochondrial membrane potential of PC-3 cells. Western blotting was used to detect the effect of AA on the expression level of mitochondrial apoptosis pathway and JAK2/STAT3 signaling pathway related proteins in PC-3 cells. Annexin V/PI method, JC-1 method and Western blotting method were used to detect the effects of JAK2 agonist Coumermycin A1 (C-A1) on mitochondrial apoptosis and expression of related proteins in PC-3 cells induced by AA. Results Compared with control group, AA significantly inhibited the proliferation of PC-3 cells in a concentration-dependent and time-dependent manner, the difference of 20—160 μmol·L^-1 group was significant (P<0.01). and the IC₅₀ value was 29.98, 23.04 and 13.81 μmol·L^-1 after 24, 48 and 72 h. AA significantly induced the apoptosis of PC-3 cells compared with control group (P<0.05 and 0.01). AA also changed the MMP in PC-3 cells. AA significantly up-regulated mitochondrial apoptosis-related Bax and cleaved Caspase 3 expression compared with control group (P<0.05 and 0.01), and significantly down-regulated mitochondrial apoptosis-related Bcl-2 expression (P<0.05 and 0.01). The phosphorylation levels of JAK2 and STAT3 in JAK2/STAT3 signaling pathway were also significantly inhibited by AA (P<0.05 and 0.01) compared with control group. Compared with AA group, AA+C-A1 significantly inhibited the apoptosis of PC-3 cells (P<0.01), inhibited the MMP in PC-3 cells significantly, significantly down-regulated Bax and cleaved Caspase 3 expression in PC-3 cells (P<0.01), and significantly up-regulated Bcl-2 expression (P<0.01), as well as significantly increased the phosphorylation levels of JAK2 and STAT3 (P<0.01). Conclusion AA could induce mitochondrial apoptosis in prostate cancer cells by inhibiting JAK2/STAT3 signaling pathway, and finally play an anti-prostate cancer role.

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江苏省自然科学基金项目（BK20191498）；国家中医管理局名医验方评价与转化重点研究室开放课题（NZYJDMF-2020001）；江苏省卫生健康委医学科研项目重点项目（ZDB2020020）