School of Pharmacy, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Faculty of materials and chemical engineering, Yibin University, Yibin, People's Republic of China.
Redox Rep. 2021 Dec;26(1):1-9. doi: 10.1080/13510002.2021.1871814.
Progression of Benign Prostate hyperplasia (BPH) is vulnerable to oxidative stress (OS) and prostatic enlargement among the aging males through apoptosis deregulation. Our present study aimed to investigate the effect of neferine (NF) in the regulation of oxidative stress and apoptosis in human BPH-1 cells.
BPH epithelial cell line BPH-1 was treated with NF for 24 and 48 h. To measure oxidative stress (OS) we investigated MDA, SOD, and GST expression along with Nrf2 and its downstream gene and protein expression. Cell proliferation and apoptosis regulation was assayed with respective methods.
Investigation revealed NF remarkably activate Nrf2 and its downstream proteins HO-1 and NQO1 at 48 h more substantially. Nrf2/Keap1 relative gene and protein expression indicated that NF might trigger Nrf2 upregulation by decreasing Keap1 expression. Both NF concentrations (3 µM and 9 µM) were able to deplete ROS and lipid peroxidation, concurrently, up-regulated SOD and GST. NF reduced cell proliferation significantly along with the regulation of apoptotic proteins Bax, Bcl2, Cyt-C, Caspase 9, and Caspase 3 at the same time (48 h).
This study is the first to manifest that NF may potentially regulate BPH by counterbalancing between OS and apoptosis through the activation of Nrf2-ARE pathway.
良性前列腺增生（BPH）的进展易受氧化应激（OS）和前列腺增大的影响，衰老男性的细胞凋亡失调。本研究旨在探讨去甲乌药碱（NF）对人 BPH-1 细胞氧化应激和细胞凋亡调节的影响。
用 NF 处理 BPH 上皮细胞系 BPH-1 24 和 48 小时。为了测量氧化应激（OS），我们研究了 MDA、SOD 和 GST 的表达，以及 Nrf2 及其下游基因和蛋白的表达。用相应的方法检测细胞增殖和凋亡调节。
研究表明，NF 在 48 小时时更显著地激活了 Nrf2 及其下游蛋白 HO-1 和 NQO1。Nrf2/Keap1 相对基因和蛋白表达表明，NF 可能通过降低 Keap1 表达来触发 Nrf2 的上调。两种 NF 浓度（3 μM 和 9 μM）均能消耗 ROS 和脂质过氧化，同时上调 SOD 和 GST。NF 显著降低细胞增殖，同时调节凋亡蛋白 Bax、Bcl2、Cyt-C、Caspase 9 和 Caspase 3（48 小时）。
本研究首次表明，NF 可能通过激活 Nrf2-ARE 通路来平衡 OS 和细胞凋亡，从而潜在地调节 BPH。
