ABSTRACT

Background

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.

Methods

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.

Results

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).

Conclusion

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.

中文翻译：

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Neferine通过Nrf2-ARE途径改善良性前列腺增生中的氧化应激和细胞凋亡。

摘要

背景

良性前列腺增生（BPH）的发展容易受到氧化应激（OS）和衰老男性中前列腺素增生的影响，这是通过细胞凋亡失调来实现的。我们目前的研究旨在调查neferine（NF）在调节人BPH-1细胞氧化应激和凋亡中的作用。

方法

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表达以及Nrf2及其下游基因和蛋白质表达。用各自的方法测定细胞增殖和凋亡调节。

结果

研究表明，NF在48小时时显着激活了Nrf2及其下游蛋白HO-1和NQO1。Nrf2 / Keap1相关基因和蛋白表达表明，NF可能通过降低Keap1表达而触发Nrf2上调。两种NF浓度（3 µM和9 µM）都能够消耗ROS和脂质过氧化，同时上调SOD和GST。NF可以同时（48小时）显着降低细胞增殖，并调节凋亡蛋白Bax，Bcl2，Cyt-C，Caspase 9和Caspase 3。

结论

该研究首次表明NF可能通过激活Nrf2-ARE途径通过平衡OS和细胞凋亡之间的作用来调节BPH。