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双去甲氧基姜黄素增强多西他赛治疗前列腺癌的疗效。

Bisdemethoxycurcumin Augments Docetaxel Efficacy for Treatment of Prostate Cancer.

机构信息

Yantai Center for Food and Drug Control.

出版信息

Biol Pharm Bull. 2024;47(8):1437-1446. doi: 10.1248/bpb.b24-00248.

Abstract

Bisdemethoxycurcumin (BDMC) is one of major forms of curcuminoids found in the rhizomes of turmeric. Docetaxel (DTX) is the standard of care for men diagnosed with androgen-independent prostate cancers. Here we report for the first time that BDMC could reinforce the effect of DTX against prostate cancer in vitro and in vivo. In vitro study, PC3 and LNCaP cells were cultured and treated with BDMC and DTX alone or in combination. The effects on cell viability were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was assessed by annexin V/propidium iodide (PI) staining, while cell cycle was assessed by PI staining. Bax, Bcl-2, caspase, poly(ADP-ribose)polymerase (PARP), cyclin B1 and CDK1 expression were assayed by Western blot. We found that a combination treatment of BDMC (10 µM) with DTX (10 nM) was more effective in the inhibition of PC3 and LNCaP cell growth and induction of apoptosis as well as G2/M arrest, which is accompanied with the significant inhibition of Bcl-2, cyclin B1, CDK1 expression and significant increase of Bax, cleaved caspase-9, cleaved caspase-3 and cleaved PARP, than those by treatment of BDMC or DTX alone. Moreover, in vivo evaluation further demonstrated the superior anticancer efficacy of BDMC and DTX compared to DTX alone in a murine prostate cancer model. These results suggest that BDMC can be an attractive therapeutic candidate in enhancing the efficacy of DTX in prostate cancer treatment.

摘要

双去甲氧基姜黄素(BDMC)是姜黄根茎中发现的主要姜黄素类化合物之一。多西他赛(DTX)是诊断为雄激素非依赖性前列腺癌的男性的标准治疗方法。在这里,我们首次报道 BDMC 可以增强 DTX 在体外和体内对前列腺癌的作用。在体外研究中,培养 PC3 和 LNCaP 细胞,并单独或联合用 BDMC 和 DTX 处理。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐(MTT)测定法测定对细胞活力的影响。通过 Annexin V/碘化丙啶(PI)染色评估细胞凋亡,通过 PI 染色评估细胞周期。通过 Western blot 测定 Bax、Bcl-2、caspase、多聚(ADP-核糖)聚合酶(PARP)、细胞周期蛋白 B1 和 CDK1 的表达。我们发现,BDMC(10 μM)与 DTX(10 nM)联合治疗更有效地抑制 PC3 和 LNCaP 细胞生长并诱导凋亡以及 G2/M 期阻滞,这伴随着 Bcl-2、细胞周期蛋白 B1、CDK1 表达的显著抑制和 Bax、裂解 caspase-9、裂解 caspase-3 和裂解 PARP 的显著增加,比单独用 BDMC 或 DTX 处理更为明显。此外,体内评估进一步证明了在小鼠前列腺癌模型中,BDMC 和 DTX 联合应用比单独应用 DTX 具有更好的抗癌疗效。这些结果表明,BDMC 可以成为增强 DTX 在前列腺癌治疗中的疗效的有吸引力的治疗候选物。

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