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

Autor: Tong Deng, Jia-Min Gu, Lan Wu, Cheng Li, Ming-Juan Zhao, Weiguang Li, Xing-Pei Guo, Xian-Tao Zeng, Cheng Fang
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Lipopolysaccharides
Male
Aging
medicine.medical_treatment
Prostatic Hyperplasia
Apoptosis
medicine.disease_cause
urologic and male genital diseases
Biochemistry
Rats
Sprague-Dawley
Prostate
Testosterone
biology
General Medicine
Hyperplasia
medicine.anatomical_structure
Cytokine
Disease Progression
Cytokines
medicine.symptom
Inflammation Mediators
Porphyromonas gingivalis
Research Article
Signal Transduction
medicine.medical_specialty
Article Subject
Inflammation
Proinflammatory cytokine
Cell Line
Internal medicine
medicine
Alveolar Process
Animals
Humans
Periodontitis
Cell Proliferation
QH573-671
business.industry
Cell Biology
medicine.disease
biology.organism_classification
Disease Models
Animal
Oxidative Stress
Endocrinology
Cytology
business
Apoptosis Regulatory Proteins
Reactive Oxygen Species
Oxidative stress
Zdroj: Oxidative Medicine and Cellular Longevity
Oxidative Medicine and Cellular Longevity, Vol 2021 (2021)
ISSN: 1942-0994
1942-0900
Popis: 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.
Databáze: OpenAIRE
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