Dataset Information

Alterations of gut microbiota diversity, composition and metabonomics in testosterone-induced benign prostatic hyperplasia rats.

ABSTRACT:

Background

Studies had shown many diseases affect the stability of human microbiota, but how this relates to benign prostatic hyperplasia (BPH) has not been well understood. Hence, this study aimed to investigate the regulation of BPH on gut microbiota composition and metabonomics.

Methods

We analyzed gut samples from rats with BPH and healthy control rats, the gut microbiota composition and metabonomics were detected by 16S rDNA sequencing and liquid chromatography tandem mass spectrometry (LC-MS/MS).

Results

High-throughput sequencing results showed that gut microbiota beta-diversity increased (P < 0.01) in the BPH group vs. control group. Muribaculaceae (P < 0.01), Turicibacteraceae (P < 0.05), Turicibacter (P < 0.01) and Coprococcus (P < 0.01) were significantly decreased in the BPH group, whereas that of Mollicutes (P < 0.05) and Prevotella (P < 0.05) were significantly increased compared with the control group. Despite profound interindividual variability, the levels of several predominant genera were different. In addition, there were no statistically significant differences in several bacteria. BPH group vs. control group: Firmicutes (52.30% vs. 57.29%, P > 0.05), Bacteroidetes (46.54% vs. 41.64%, P > 0.05), Clostridia (50.89% vs. 54.66%, P > 0.05), Ruminococcaceae (25.67% vs. 20.56%, P > 0.05). LC-MS/MS of intestinal contents revealed that differential metabolites were mainly involved in cellular processes, environmental information processing, metabolism and organismal systems. The most important pathways were global and overview maps, lipid metabolism, amino acid metabolism, digestive system and endocrine system. Through enrichment analysis, we found that the differential metabolites were significantly enriched in metabolic pathways, steroid hormone biosynthesis, ovarian steroidogenesis, biosynthesis of unsaturated fatty acids and bile secretion. Pearson correlation analysis (R = 0.94) showed that there was a strong correlation between Prevotellaceae, Corynebacteriaceae, Turicibacteraceae, Bifidobacteriaceae and differential metabolites.

Conclusion

Our findings suggested an association between the gut microbiota and BPH, but the causal relationship between the two groups is unclear. Thus, further studies are warranted to elucidate the potential mechanisms and causal relationships between BPH and gut microbiota.

SUBMITTER: Li LY

PROVIDER: S-EPMC8962033 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature

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Publications

Alterations of gut microbiota diversity, composition and metabonomics in testosterone-induced benign prostatic hyperplasia rats.

Li Lu-Yao LY Han Jie J Wu Lan L Fang Cheng C Li Wei-Guang WG Gu Jia-Min JM Deng Tong T Qin Chang-Jiang CJ Nie Jia-Yan JY Zeng Xian-Tao XT

Military Medical Research 20220328 1

<h4>Background</h4>Studies had shown many diseases affect the stability of human microbiota, but how this relates to benign prostatic hyperplasia (BPH) has not been well understood. Hence, this study aimed to investigate the regulation of BPH on gut microbiota composition and metabonomics.<h4>Methods</h4>We analyzed gut samples from rats with BPH and healthy control rats, the gut microbiota composition and metabonomics were detected by 16S rDNA sequencing and liquid chromatography tandem mass sp ...[more]

PMID: 35346378

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Project description:IntroductionBenign prostatic hyperplasia (BPH) is a common disease among elderly men. Its pharmacological treatment is still unsatisfactory. 6-Paradol (6-PD) is an active metabolite found in many members of the Zingiberaceae family. It was reported to possess anti-proliferative, antioxidant, and anti-inflammatory activities. The present study aimed at exploring the potential of 6-PD to inhibit testosterone-induced BPH in rats as well as the probable underlying mechanism.MethodsMale Wistar rats were divided into 6 groups and treated as follows: Group 1 (control group) received vehicles only, Group 2 testosterone only, Groups 3 and 4 received 6-PD (2.5 and 5.0 mg/kg; respectively) and testosterone, and Group 6 received finasteride and testosterone.ResultsDaily treatment of animals with 6-PD at the two dose levels of 2.5 and 5 mg/kg significantly ameliorated a testosterone-induced rise in prostate index and weight. This was confirmed by histological examinations of prostatic tissues that indicated a reduction in the pathological changes as well as inhibition of the rise in glandular epithelial height in 6-PD treated rats. Immunohistochemical investigations showed that 6-PD prevented the up-regulation of cyclin D1 induced by testosterone injections. Further, 6-PD significantly modulated mRNA expression of both Bcl2 and Bax in prostate tissues of testosterone-treated rats in favor of anti-proliferation. It also showed antioxidant activities as evidenced by inhibition of accumulation of malondialdehyde (MDA) and exhaustion of catalase (CAT) activity. In addition, 6-PD displayed significant anti-inflammatory activities as it prevented up-regulation of interleukin-6 (IL-6) and nuclear factor kappa B (NF-κB). Immunoblotting analysis revealed that 6-PD significantly inhibited testosterone-induced activation of AKT and mTOR in prostate tissues.Conclusions6-PD protects against testosterone-induced BPH in rats. This can be attributed, at least partly, to its antiproliferative, antioxidant, and anti-inflammatory properties as well as its ability to inhibit activation of the AKT/mTOR axis.

Project description:BackgroundRecent researches have shown a correlation between the gut microbiota (GM) and various diseases. However, it remains uncertain whether the relationship between GM and benign prostatic hyperplasia (BPH) is causal.MethodsWe carried out a two-sample Mendelian randomization (MR) analysis, utilizing data from the most extensive GM-focused genome-wide association study by the MiBioGen consortium, with a sample size of 13,266. Data for BPH, encompassing 26,358 cases and 110,070 controls, were obtained from the R8 release of the FinnGen consortium. We employed multiple techniques, such as inverse variance weighted (IVW), constrained maximum likelihood and model averaging methods, maximum likelihood, MR-Pleiotropy RESidual Sum and Outlier (MRPRESSO),MR-Egger, and weighted median methods, to investigate the causal relationship between GM and BPH. To evaluate the heterogeneity among the instrumental variables, Cochran's Q statistics were employed. Additionally, the presence of horizontal pleiotropy was assessed through the application of both MR-Egger and MR-PRESSO tests. The direction of causality was scrutinized for robustness using the MR-Steiger directionality test. A reverse MR analysis examined the GM previously linked to BPH through a causal relationship in the forward MR assessment.ResultsAccording to the analysis conducted using IVW,Eisenbergiella (odds ratio [OR]=0.92, 95% confidence interval [CI]: 0.85-0.99,P=0.022) and Ruminococcaceae (UCG009) (OR=0.88, 95% CI: 0.79-0.99, P=0.027) were found to reduce the risk of BPH, while Escherichia shigella (OR=1.19, 95% CI: 1.05-1.36, P=0.0082) appeared to increase it. The subsequent reverse MR analysis revealed that the three GM were not significantly influenced by BPH, and there was no noticeable heterogeneity or horizontal pleiotropy among the instrumental variables.Conclusion: These results indicated a causal relationship between Eisenbergiella, Ruminococcaceae (UCG009), and Escherichia shigella and BPH. Further randomized controlled trials are needed to explore more comprehensively the roles and operational mechanisms of these GM in relation to BPH.

Dataset Information

Alterations of gut microbiota diversity, composition and metabonomics in testosterone-induced benign prostatic hyperplasia rats.

Background

Methods

Results

Conclusion

Publications

Alterations of gut microbiota diversity, composition and metabonomics in testosterone-induced benign prostatic hyperplasia rats.

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