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Bunge 通过激活 Nrf-2/HO-1 来调节氧化应激改善良性前列腺增生。

Bunge Ameliorates Benign Prostatic Hyperplasia through Regulation of Oxidative Stress via Nrf-2/HO-1 Activation.

机构信息

Department of Food Science and Nutrition, Dong-A University, Busan 49315, Republic of Korea.

Department of Health Sciences, the Graduate School of Dong-A University, Busan 49315, Republic of Korea.

出版信息

J Microbiol Biotechnol. 2024 May 28;34(5):1059-1072. doi: 10.4014/jmb.2308.08053. Epub 2023 Oct 31.

DOI:10.4014/jmb.2308.08053
PMID:37994101
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11180924/
Abstract

Oxidative stress is a key factor in the pathogenesis of benign prostatic hyperplasia (BPH) that leads to inflammation. This study aimed to evaluate the ameliorative effects of Bunge extract (HLT-101) on BPH through the regulation of oxidative stress and inflammation. A testosterone propionate (TP)-induced BPH rat model was orally administered HLT-101 (20, 40, or 80 mg/kg), and its effects on oxidative stress- and inflammation-related gene expression were examined. Further, HLT-101 was assessed for its effect on reactive oxygen species (ROS) levels and Nrf-2/HO-1 signaling pathways in BPH-1 cells. HLT-101 decreased testosterone-induced excessive free radical production and inflammatory factor activation. Moreover, HLT-101 treatment significantly decreased the intracellular ROS level in the TNF-α and IFN-γ treated BPH-1 cells through the activation of Nrf-2. In addition, HLT-101 treatment inhibited the NF-κB pathway and androgen receptor (AR) signaling, which is highly linked to the pathogenesis of BPH. Therefore, HLT-101 has the potential to be an effective treatment reagent for BPH because of its ability to reduce inflammation and oxidative stress via Nrf-2/HO-1 signaling.

摘要

氧化应激是导致良性前列腺增生(BPH)炎症的关键因素。本研究旨在评估 Bunge 提取物(HLT-101)通过调节氧化应激和炎症对 BPH 的改善作用。通过给予丙酸睾酮(TP)诱导的 BPH 大鼠口服 HLT-101(20、40 或 80mg/kg),并检测其对氧化应激和炎症相关基因表达的影响。进一步评估 HLT-101 对 BPH-1 细胞中活性氧(ROS)水平和 Nrf-2/HO-1 信号通路的影响。HLT-101 可降低睾酮诱导的过多自由基产生和炎症因子激活。此外,HLT-101 通过激活 Nrf-2,显著降低 TNF-α和 IFN-γ处理的 BPH-1 细胞中的细胞内 ROS 水平。此外,HLT-101 可抑制 NF-κB 途径和雄激素受体(AR)信号通路,这与 BPH 的发病机制密切相关。因此,HLT-101 通过 Nrf-2/HO-1 信号通路减轻炎症和氧化应激,具有成为 BPH 有效治疗试剂的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54ec/11180924/4603f932a835/jmb-34-5-1059-f8.jpg
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