AKR1B10 expression in benign prostatic hyperplasia and its related mechanism

Xu,Wenjing; Gao,Ya; Zhang,Jiaqi; Zhang,Rong; Chen,Qihua

doi:10.3892/ol.2021.12944

AKR1B10 expression in benign prostatic hyperplasia and its related mechanism

Authors:
- Wenjing Xu
- Ya Gao
- Jiaqi Zhang
- Rong Zhang
- Qihua Chen
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Affiliations: First Clinical College of Chinese Medicine, Hunan University of Chinese Medicine, Changsha, Hunan 410208, P.R. China, Department of Proctology, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, P.R. China, First Clinical College of Chinese Medicine, Hunan University of Chinese Medicine, Changsha, Hunan 410208, P.R. China, Department of Surgery and Male Disease, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, P.R. China
Published online on: July 27, 2021 https://doi.org/10.3892/ol.2021.12944
Article Number: 683
Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the present study was to investigate the expression of aldo‑keto reductase family 1 member B10 (AKR1B10) in benign prostatic hyperplasia (BPH) and its related mechanism. In total, 142 BPH patients admitted from March 2017 to March 2019 at the First Hospital of Hunan University of Chinese Medicine and 140 healthy people undergoing physical examination were selected as the research subjects. The clinical value of AKR1B10 in BPH was analyzed. Twenty clean SD rats were selected, and 10 were selected to establish the prostate hyperplasia model, while the remaining 10 were set as the control group. Ten days after the model was established, AKR1B10 and NF‑κB expression in prostate tissues of rats in both groups was detected by PCR and immunohistochemistry. The primary cells in prostate hyperplasia were cultured, and then they were transfected with AKR1B10 to observe the changes of cell biological behavior. AKR1B10 and NF‑κB mRNA significantly increased in peripheral blood of BPH patients and prostate tissue of BPH model rats (P<0.001), and AKR1B10 had good diagnostic value for BPH (P<0.001). In addition, it was positively correlated with PSA, EGF, IL‑6 and TNF‑α (P<0.001). After transfection with AKR1B10‑inhibitor, it was revealed that the proliferation of prostate hyperplasia cells decreased, while the apoptosis of prostate hyperplasia cells increased and the NF‑κB protein expression decreased (P<0.001). Collectively, high expression of AKR1B10 in BPH promoted the proliferation of prostate cells and reduced their apoptosis, and the mechanism may be through regulation of NF‑κB.

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