Abstract

Context

Inflammation and epithelial-mesenchymal transition (EMT) play important roles in the occurrence and development of benign prostatic hyperplasia (BPH); curcumin exerts anti-proliferative, anti-inflammatory, and anti-EMT effects.

Objective

To explore the anti-inflammatory and anti-EMT mechanisms of curcumin in BPH.

Materials and methods

Ten-week-old male C57BL/6 mice were administered lipopolysaccharide (LPS, 100 µg/kg) in the prostate lobules to establish an inflammatory BPH model (LPS group), and curcumin (120 mg/kg) was administered into the abdominal cavity for 2 weeks (three times a week, curcumin-treated group). A group of healthy mice served as the control group. The expression of Toll-like receptor 4 (TLR4), bone morphogenetic protein and activin membrane-bound inhibitor (BAMBI), EMT markers, inflammatory cytokines, and transforming growth factor β1 (TGF-β1) was detected by PCR and western blotting. TGF-β1 (0.1 ng/mL) and LPS (100 ng/mL) were used to induce EMT in benign prostatic hyperplasia epithelial cells (BPH-1).

Results

In vivo, curcumin reduced the size of the prostate, suppressed the expression of vimentin and TLR4, and increased the expression of E-cadherin and BAMBI in the LPS-induced BPH mouse model. Moreover, curcumin decreased the levels of IL-6 and TNF-α by 44.52 and 46.17%, respectively. In vitro, curcumin attenuated cell proliferation, suppressed the expression of vimentin and TLR4, and increased the expression of E-cadherin and BAMBI in BPH-1 cells. Furthermore, BAMBI knockdown reversed the expression of vimentin and E-cadherin induced by curcumin.

Discussion and conclusion

This study demonstrated that curcumin alleviated hyperplasia, EMT, and inflammation in vivo. Furthermore, curcumin suppressed EMT by targeting BAMBI via the TLR4/BAMBI/TGF-β1 signalling pathway in vitro, demonstrating its potential utility in BPH treatment.

中文翻译：

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姜黄素通过上调骨形态发生蛋白和激活素膜结合抑制剂减轻炎症引起的前列腺增生

摘要

语境

炎症和上皮间质转化（EMT）在良性前列腺增生（BPH）的发生发展中起重要作用；姜黄素具有抗增殖、抗炎和抗 EMT 作用。

客观的

探讨姜黄素在 BPH 中的抗炎和抗 EMT 机制。

材料和方法

10周龄雄性C57BL/6小鼠前列腺小叶给予脂多糖（LPS，100 μg/kg）建立炎症性BPH模型（LPS组），腹腔给予姜黄素（120 mg/kg） 2 周（每周 3 次，姜黄素治疗组）。一组健康小鼠作为对照组。通过PCR和蛋白质印迹检测Toll样受体4（TLR4）、骨形态发生蛋白和激活素膜结合抑制剂（BAMBI）、EMT标志物、炎性细胞因子和转化生长因子β1（TGF-β1）的表达。TGF-β1 (0.1 ng/mL) 和 LPS (100 ng/mL) 用于在良性前列腺增生上皮细胞 (BPH-1) 中诱导 EMT。

结果

在体内，姜黄素在 LPS 诱导的 BPH 小鼠模型中减小了前列腺的大小，抑制了波形蛋白和 TLR4 的表达，并增加了 E-cadherin 和 BAMBI 的表达。此外，姜黄素使 IL-6 和 TNF-α 水平分别降低了 44.52% 和 46.17%。在体外，姜黄素减弱细胞增殖，抑制波形蛋白和 TLR4 的表达，并增加 BPH-1 细胞中 E-cadherin 和 BAMBI 的表达。此外，BAMBI 敲低逆转了姜黄素诱导的波形蛋白和 E-钙粘蛋白的表达。

讨论与结论

这项研究表明，姜黄素可以减轻体内的增生、EMT 和炎症。此外，姜黄素在体外通过 TLR4/BAMBI/TGF-β1 信号通路靶向 BAMBI 抑制 EMT ，证明了其在 BPH 治疗中的潜在用途。