scholarly journals Oxidative stress promotes benign prostatic hyperplasia

The Prostate ◽  
2015 ◽  
Vol 76 (1) ◽  
pp. 58-67 ◽  
Author(s):  
Paz Vital ◽  
Patricia Castro ◽  
Michael Ittmann
Keyword(s):  
Oxidative Stress ◽  
Benign Prostatic Hyperplasia ◽  
Prostatic Hyperplasia

Diacerein ameliorates testosterone-induced benign prostatic hyperplasia in rats: Effect on oxidative stress, inflammation and apoptosis

2021 ◽  
Vol 100 ◽  
pp. 108082
Author(s):  
Mohamed El-Sherbiny ◽  
Mohamed El-Shafey ◽  
Mosaab Salah El-din El-Agawy ◽  
Abdelaty Shawky Mohamed ◽  
Nada H. Eisa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Benign Prostatic Hyperplasia ◽  
Prostatic Hyperplasia

scholarly journals PROFILE IN GANGLIOSIDE ANTIBODIES IN BENIGN PROSTATIC HYPERPLASIA

2016 ◽  
Vol 15 (1) ◽  
pp. 30-34
Author(s):  
Ilinca Nicolae ◽  
◽  
Corina-Daniela Ene ◽  
Mirela Petrescu ◽  
Simona Roxana Georgescu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Benign Prostatic Hyperplasia ◽  
Prostatic Hyperplasia ◽  
Careful Monitoring ◽  
Ganglioside Antibodies ◽  
Immunological Interactions ◽  
Potential Risk Factors ◽  
Inflammatory Neuropathies ◽  
Infectious Etiology

Molecular pathology of benign prostatic hyperplasia is multifactorial and involves endocrine, biochemical, immunological interactions. The mechanisms involved in the onset and progression of benign prostatic hyperplasia are: infections, older than 50 years, imbalances in hormones and neurotransmitters, inflammation, oxidative stress. It is estimated that an infectious etiology can be a cause of wrong immune response directed at the prostate. Inflammatory neuropathies often occur after infections with various microorganisms. It is also known, that the presence of microorganisms is heterogeneous in patients with benign prostatic hyperplasia. In this paper we documented the antibody profile of anti-GM1, -GM2, -GM3, -GD1a, -GD1b, -GT1b, -GQ1b IgG and IgM type in 30 patients with benign prostatic hyperplasia and in 30 controls. The results showed an increasing anti-GD1a and anti-GQ1b titer in patients with benign prostatic hyperplasia compared to control. The authors suggest that a careful monitoring of the patients developing an endogenous anti-gangliosidic immune response is required in order to assess these antibodies as potential risk factors for neuropathy in patients with benign prostatic hyperplasia.

scholarly journals Role of gangliosides in prostate pathology

2016 ◽  
Vol 19 (1) ◽  
pp. 10-15
Author(s):  
Ilinca Nicolae ◽  
◽  
Corina-Daniela Ene ◽  
Simona Roxana Georgescu ◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Differential Diagnosis ◽  
Benign Prostatic Hyperplasia ◽  
Molecular Pathology ◽  
Potential Role ◽  
Prostatic Hyperplasia ◽  
Immunologic Markers ◽  
Immunological Interactions

Molecular pathology of benign prostatic hyperplasia is multifactorial and involves endocrine, biochemical, immunological interactions. The mechanisms involved in the onset and progression of benign prostatic hyperplasia are: infections, 50 years of age, hormones and neurotransmitters imbalances, inflammation, oxidative stress. The potential role of glycosylation in the pathogenesis of prostate disease has been neglected. In this study we documented the profile of gangliosides in normal and pathological prostatic tissues together with the pathologic changes seen in the level of extracellular gangliosides in patients with prostate pathology. Analysis of the data in the literature suggests that gangliosides may represent immunologic markers useful in the differential diagnosis between prostate cancer and benign prostatic hyperplasia.

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

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yanbo Chen ◽  
Hui Xu ◽  
Chong Liu ◽  
Meng Gu ◽  
Qi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Benign Prostatic Hyperplasia ◽  
Prostatic Hyperplasia ◽  
Therapeutic Effects ◽  
Prostate Cell ◽  
Mesenchymal Transition ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D

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.

scholarly journals Periodontitis Exacerbates Benign Prostatic Hyperplasia through Regulation of Oxidative Stress and Inflammation

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Cheng Fang ◽  
Lan Wu ◽  
Ming-Juan Zhao ◽  
Tong Deng ◽  
Jia-Min Gu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Benign Prostatic Hyperplasia ◽  
Histological Examination ◽  
Alveolar Bone ◽  
Epidemiological Studies ◽  
In Vitro Models ◽  
Prostatic Hyperplasia ◽  
Control Group ◽  
Periodontal Tissues

Epidemiological studies demonstrate that men with periodontitis are also susceptible to benign prostatic hyperplasia (BPH) and that periodontal treatment can improve the prostatic symptom. However, molecular links of this relationship are largely unknown. The goal of the current study was to elucidate the effects of experimental periodontitis on the hyperplasia of prostate and whether oxidative stress and inflammation participated in this process. For this purpose, ligature-induced periodontitis, testosterone-induced BPH, and the composite models in rats were established. Four weeks later, all the rats were sacrificed and the following items were measured: alveolar bone loss and histological examination of periodontal tissues were taken to assess the establishment of periodontitis model, prostate index and histological examination of prostate tissues were taken to test the establishment of the BPH model, inflammatory cytokines in plasma were assessed, and Bax/Bcl-2 proteins related to cell apoptosis were analyzed via western blot analysis. To further investigate whether oxidative stress participates in the aggravation of BPH, in vitro models were also conducted to measure the production of intracellular reactive oxygen species (ROS) and hydrogen peroxide (H2O2) concentration. We found that simultaneous periodontitis and BPH synergistically aggravated prostate histological changes, significantly increased Ki67 proliferation, and reduced apoptosis in rat prostate tissues. Also, our results showed that periodontal ligation induced increased Bcl-2 protein expression, whereas Bax expression was decreased in BPH rats than in normal rats. Compared with the control group, periodontitis and BPH both significantly enhanced inflammatory cytokine levels of TNF-α, IL-6, IL-1β, and CRP. Furthermore, Porphyromonas gingivalis lipopolysaccharide induced enhanced generation of intracellular expression of ROS and H2O2 in BPH-1 cells. Our experimental evidence demonstrated that periodontitis might promote BPH development through regulation of oxidative stress and inflammatory process, thus providing new strategies for prevention and treatment of BPH.

Oxidative Stress in Benign Prostatic Hyperplasia and Prostate Cancer

2010 ◽  
Vol 85 (3) ◽  
pp. 328-333 ◽  
Author(s):  
Gianna Pace ◽  
Caterina Di Massimo ◽  
Daniela De Amicis ◽  
Carlo Corbacelli ◽  
Laura Di Renzo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Prostatic Hyperplasia

Oxidative Stress in Benign Prostatic Hyperplasia: A Systematic Review

2014 ◽  
Vol 94 (3) ◽  
pp. 249-254 ◽  
Author(s):  
Paola Lucia Minciullo ◽  
Antonino Inferrera ◽  
Michele Navarra ◽  
Gioacchino Calapai ◽  
Carlo Magno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Free Radicals ◽  
Benign Prostatic Hyperplasia ◽  
Defense Mechanisms ◽  
Cellular Proliferation ◽  
Prostatic Hyperplasia ◽  
Dietary Factors ◽  
Key Words Oxidative Stress

Background: Several parameters including inflammatory mediators, hormones, dietary factors, inflammatory genes, and oxidative stress (OS) have been considered to play a role in the development of benign prostatic hyperplasia (BPH). Prostate tissue damage and OS may lead to compensatory cellular proliferation with resulting hyperplastic growth. Methods: We searched MEDLINE for articles in English published up to March 2014 using the key words ‘oxidative stress', ‘antioxidants' and ‘benign prostatic hyperplasia'. Results: Prostatic inflammation can cause the generation of free radicals. The extent of oxidative damage can be exacerbated by a decreased efficiency of antioxidant defense mechanisms. The balance between OS and the antioxidant component also has a role in developing prostate disease. Several works show the role of oxidant products and of depletion of antioxidant substances in BPH patients. It is accepted that free radicals play a role in carcinogenesis and that BPH should be considered a premalignant condition which may evolve into prostate cancer. High OS parameters and low antioxidant activity are more prominent in prostate cancer patients compared with BPH and controls. Conclusions: Further studies are needed to clarify the potential role of antioxidants in BPH also in view of preventing the progression to prostate cancer.

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