Protocatechuic acid ameliorates testosterone‐induced benign prostatic hyperplasia through the regulation of inflammation and oxidative stress in castrated rats

2020 ◽  
Vol 34 (8) ◽  
Author(s):  
Olubukola O. Akanni ◽  
Solomon E. Owumi ◽  
Olusegun G. Olowofela ◽  
Adebukola A. Adeyanju ◽  
Olusoji J. Abiola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Benign Prostatic Hyperplasia ◽  
Protocatechuic Acid ◽  
Prostatic Hyperplasia ◽  
And Oxidative Stress

scholarly journals Palmitoylethanolamide/Baicalein Regulates the Androgen Receptor Signaling and NF-κB/Nrf2 Pathways in Benign Prostatic Hyperplasia

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1014
Author(s):  
Ramona D’Amico ◽  
Tiziana Genovese ◽  
Marika Cordaro ◽  
Rosalba Siracusa ◽  
Enrico Gugliandolo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Androgen Receptor ◽  
Benign Prostatic Hyperplasia ◽  
Fixed Ratio ◽  
Prostatic Hyperplasia ◽  
Prostate Cell ◽  
Common Benign Tumor ◽  
Markers Of Inflammation ◽  
Ultramicronized Palmitoylethanolamide ◽  
And Oxidative Stress

Benign prostatic hyperplasia (BPH) is the most common benign tumor in males. Androgen/androgen receptor (AR) signaling plays a key role in the development of BPH; its alterations cause an imbalance between prostate cell growth and apoptosis. Furthermore, chronic inflammation and oxidative stress, which are common conditions in BPH, contribute to disrupting the homeostasis between cell proliferation and cell death. With this background in mind, we investigated the effect of ultramicronized palmitoylethanolamide (um-PEA), baicalein (Baic) and co-ultramicronized um-PEA/Baic in a fixed ratio of 10:1 in an experimental model of BPH. BPH was induced in rats by daily administration of testosterone propionate (3 mg/kg) for 14 days. Baic (1 mg/kg), um-PEA (9 mg/kg) and um-PEA/Baic (10 mg/kg) were administered orally every day for 14 days. This protocol led to alterations in prostate morphology and increased levels of dihydrotestosterone (DHT) and of androgen receptor and 5α-reductase expression. Moreover, testosterone injections induced a significant increase in markers of inflammation, apoptosis and oxidative stress. Our results show that um-PEA/Baic is capable of decreasing prostate weight and DHT production in BPH-induced rats, as well as being able to modulate apoptotic and inflammatory pathways and oxidative stress. These effects were most likely related to the synergy between the anti-inflammatory properties of um-PEA and the antioxidant effects of Baic. These results support the view that um-PEA/Baic should be further studied as a potent candidate for the management of BPH.

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.

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
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