Therapeutic Effects of 25-Hydroxyvitamin D on the Pathological Process of Benign Prostatic Hyperplasia: An In Vitro Evidence.

Yanbo Chen,Chong Liu,Meng Gu,Zhong Wang,Ming Zhan,Qi Chen,Hui Xu,Michele Malaguarnera

doi:10.1155/2021/4029470

Yanbo Chen, Chong Liu + Show 6 more

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https://doi.org/10.1155/2021/4029470

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Journal: Disease markers	Publication Date: Oct 11, 2021
Citations: 4	License type: CC BY 4.0

Affiliation: Shanghai Ninth People's Hospital

Abstract

The pathogenesis of benign prostatic hyperplasia (BPH) is extremely complicated which involving the multiple signaling pathways. The deficiency of vitamin D is an important risk factor for BPH, and exogenous vitamin D is effective for the treatment of BPH. In this study, we provided in vitro mechanical evidence of vitamin D as a treatment for BPH using BPH-1, WPMY-1, and PBMC cells. We found that 25-hydroxyvitamin D (25-OH D) level is decreased in BPH and closely correlated with age, prostate volume, maximum flow, international prostate symptom score, and prostate-specific antigen of the BPH patients. We further revealed that 25-OH D ameliorated TGF-β1 induces epithelial-mesenchymal transition (EMT) of BPH-1 cells and proliferation of WPMY-1 cells via blocking TGF-β signaling. Moreover, 25-OH D was able to block NF-κB signaling in PBMCs of BPH patients and STAT3 signaling in BPH cells to relieve inflammation. 25-OH D also protects BPH cells from inflammatory cytokines selected by PBMCs. Finally, we uncovered that 25-OH D alleviated prostate cell oxidative stress by triggering Nrf2 signaling. In conclusion, our data verified that 25-OH D regulated multiple singling pathways to restrain prostate cell EMT, proliferation, inflammation, and oxidative stress. Our study provides in vitro mechanical evidence to support clinical use of vitamin D as a treatment for BPH.

Highlights

Benign prostatic hyperplasia (BPH) is a chronic progressive condition which impacts a substantial number of older men [1, 2]
The results showed that the phosphorylation as well as the transcriptional activity of STAT3 in both Benign prostatic hyperplasia epithelial-1 (BPH-1) cells and WPMY-1 cells was significantly upregulated by cell supernatant of Peripheral blood mononuclear cells (PBMCs) and attenuated by 25-hydroxyvitamin D (25-OH D) (Figures 2(i)–2(l))
These results indicated that 25-OH D was able to block NF-κB signaling in PBMCs of BPH patients and STAT3 signaling in BPH cells to relieve inflammation. 25-OH D protects BPH cells from inflammatory cytokines selected by PBMCs

Summary

Introduction

Benign prostatic hyperplasia (BPH) is a chronic progressive condition which impacts a substantial number of older men [1, 2]. Many risk factors including, aging, inflammation, hormones, oxidative stress, physical activity, and dietary factors are considered to participate in BPH development, leading to the pathogenesis of BPH extremely multifactorial [5]. Oxidative stress is considered to play a role in the development of BPH, in which Nrf signaling is deficient and insufficient for antioxidant response [11, 12]. Interfering the activation of these signaling may produce therapeutic effects on the pathogenesis of BPH. Accumulating evidence indicates that low vitamin D, especially the active 25-hydroxyvitamin D (25-OH D), is deficient in BPH patients and may be closely associated with the disease pathophysiologic processes [14, 15]. In this study, we want to conduct in vitro experiments to further investigate the mechanism of vitamin D as a treatment for BPH

Materials and Methods

Results

Findings

Discussion