International Journal of Men''s Social and Community Health最新文献

{"title":"Exploring the mechanism of Bu Zhong Yi Qi Tang in the treatment of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) based on network pharmacology and molecular docking","authors":"Pengfei Zhou, Yang Xuan, Zaisheng Zhu, Han Wu, Yang Hu, Liangyou Chen, Qianya Zhou","doi":"10.22514/jomh.2025.039","DOIUrl":"https://doi.org/10.22514/jomh.2025.039","url":null,"abstract":"Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common and persistent condition affecting the male urinary system, with a global prevalence ranging from 2% to 10%. This study aims to investigate the therapeutic mechanisms of Bu Zhong Yi Qi Tang (BZYQT) in treating CP/CPPS using network pharmacology and molecular docking techniques. Methods: The active compounds and their corresponding target proteins of BZYQT were identified and screened using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). Targets associated with CP/CPPS were determined through GeneCards, the Therapeutic Target Database (TTD), Online Mendelian Inheritance in Man (OMIM), and the Pharmacogenomics Knowledgebase (PharmGKB). Overlapping targets between BZYQT and CP/CPPS were analyzed using the STRING database to construct a protein-protein interaction (PPI) network. Key targets were further subjected to Gene Ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Molecular docking studies were conducted to validate the interactions between core active compounds and key targets. In vitro experiments were performed to confirm the therapeutic efficacy of BZYQT in treating CP/CPPS. Results: The study identified 103 active compounds in BZYQT and 2064 potential target proteins. A total of 1020 CP/CPPS-related targets were retrieved from GeneCards, OMIM, TTD, and PharmGKB, leading to the identification of 73 overlapping targets and 5 core targets. GO enrichment analysis revealed that these targets are involved in inflammatory responses, apoptosis, oxidative stress, and cell proliferation. KEGG pathway analysis highlighted associations with pathways such as the ErbB signaling pathway. Molecular docking results suggested that kaempferol, an active compound in BZYQT, exhibited the highest binding affinity with the target proteins. Experimental validation demonstrated that kaempferol effectively inhibited the expression of EGFR, MMP9, TNF-α, and IL-6. Conclusions: BZYQT exhibits significant therapeutic potential in the treatment of CP/CPPS through its multi-target and multi-pathway mechanisms. The active compound kaempferol plays a crucial role in alleviating pathological changes in CP/CPPS by downregulating the expression of MMP9, EGFR, IL-6, and TNF-α. These findings provide a molecular basis for the application of traditional Chinese medicine in the management of CP/CPPS.","PeriodicalId":52382,"journal":{"name":"International Journal of Men''s Social and Community Health","volume":"21 3","pages":"77-77"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147877801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The toxicity and mechanisms of pyrotinib on male reproductive system","authors":"Xiao Hu, Zhongjian Pan, Jie Yang, Peng Zheng, Jian Tan, Zhipeng Xu, Huaming Tang, Jianpeng Hu","doi":"10.22514/jomh.2025.102","DOIUrl":"https://doi.org/10.22514/jomh.2025.102","url":null,"abstract":"Background: While Pyrotinib is effective in treating human epidermal growth factor receptor 2 (HER2)-positive breast cancer, its impact on male reproductive health remains unclear. This study investigates the potential reproductive toxicity and underlying mechanisms of Pyrotinib in male Leydig cells, key regulators of testosterone production. Methods: Leydig cells were treated with Pyrotinib, with 0.1‰ dimethyl sulfoxide (DMSO)-treated cells serving as the control group, to evaluate its effects on cell viability, apoptosis, cell cycle progression and signaling pathways. Clonogenic assays, flow cytometry, Western blotting and transcriptome sequencing were employed. Results: Pyrotinib treatment for 24 hours significantly reduced cell viability and colony formation while increasing apoptosis. Flow cytometry revealed G1 phase arrest in 67.2% of cells after Pyrotinib exposure. Western blot analysis showed transient activation of Ak strain transforming (AKT) and extracellular signal-regulated kinase (ERK) at 2 hours, followed by marked inhibition at 24–48 hours. Transcriptomic analysis identified 197 downregulated genes enriched in chromatin organization and mitotic processes, particularly cell cycle regulation. Conclusions: Pyrotinib impairs Leydig cell proliferation through G1 arrest and inhibition of the phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK)/ERK pathways, along with downregulation of cell cycle-related genes. These findings highlight the need for further evaluation of Pyrotinib’s reproductive safety in male patients.","PeriodicalId":52382,"journal":{"name":"International Journal of Men''s Social and Community Health","volume":"21 7","pages":"107-107"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147902411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LRRC15 accelerates lung adenocarcinoma cells' proliferation and chemoresistance","authors":"Chen Hua, Haiyan Bian, Yuejun Sun","doi":"10.22514/jomh.2025.133","DOIUrl":"https://doi.org/10.22514/jomh.2025.133","url":null,"abstract":"Background: Lung adenocarcinoma (LUAD) is one of the most common malignant tumors and poses a serious threat to patient health and survival. Leucine-rich repeat-containing protein 15 (LRRC15) has been reported to act as a promoter in certain cancers, and importantly, its expression has been found to be elevated in LUAD. Methods: Protein expression was examined using immunohistochemistry (IHC, n = 6 for tissues) and Western blotting. Cell survival rate (%) and half-maximal inhibitory concentration (IC50) were assessed using the Cell Counting Kit (CCK)-8 assay. Cell proliferation was evaluated through colony formation assays. Results: LRRC15 expression was significantly upregulated in LUAD tissues and cell lines, and was associated with poor prognosis. Knockdown of LRRC15 inhibited cell proliferation, and suppression of LRRC15 reduced cisplatin resistance by limiting autophagy. Furthermore, it was demonstrated that LRRC15 promoted autophagy through activation of Unc-51-like autophagy-activating kinase 1 (ULK1). Conclusions: These findings indicate that LRRC15 may enhance both proliferation and chemoresistance of LUAD cells by triggering ULK1-mediated autophagy. Therefore, LRRC15 may represent a potential therapeutic target for improving LUAD treatment outcomes.","PeriodicalId":52382,"journal":{"name":"International Journal of Men''s Social and Community Health","volume":"21 11","pages":"37-37"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147922827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of CUEDC1 restrains the growth and migration of hepatocellular carcinoma cells through affecting the TβRI/Smad signaling pathway","authors":"Jin Wang, Zhenglan Cao, Kehong Chen","doi":"10.22514/jomh.2024.061","DOIUrl":"https://doi.org/10.22514/jomh.2024.061","url":null,"abstract":"Hepatocellular carcinoma (HCC), as one usual tumor, and owns the significant mortality rates. The involvement of the coupling of ubiquitin conjugation to endoplasmic reticulum degradation (CUE) domain containing 1 (CUEDC1) in cancer progression, either facilitating or inhibiting, has been documented in various cancers. Nevertheless, the regulatory role of CUEDC1 in HCC progression holds unclear. This work aims to elucidate the impact of CUEDC1 on HCC progression. Analysis using the Gene Expression Profiling Interactive Analysis (GEPIA) online database revealed elevated expression of CUEDC1 in liver hepatocellular carcinoma (LIHC) tissues. Subsequently, in HCC cell lines, the elevated CUEDC1 protein expression was confirmed. Silencing CUEDC1 was found to restrain tumor growth in HCC, alongside attenuating cell migration and invasion. Notably, knockdown of CUEDC1 was determined to activate the transforming growth factor-β receptor I (TβRI)/Smad signaling pathway. In conclusion, this study demonstrates that CUEDC1 knockdown restrained the growth and migration of HCC cells under affecting the TβRI/Smad signaling pathway. These findings suggest CUEDC1 could be a helpful target for HCC improvement.","PeriodicalId":52382,"journal":{"name":"International Journal of Men''s Social and Community Health","volume":"20 4","pages":"127-127"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://oss.jomh.org/files/article/20240429-259/pdf/JOMH2024032501.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"POU2F2 aggravates cell proliferation and autophagy in lung adenocarcinoma","authors":"Ronggang Luo, Yi Zhuo, Quan Du, Rendong Xiao","doi":"10.22514/jomh.2024.113","DOIUrl":"https://doi.org/10.22514/jomh.2024.113","url":null,"abstract":"Lung adenocarcinoma (LUAD) is one deadly tumor with high incidence. POU class 2 homeobox 2 (POU2F2) has been notarized to exhibit roles in the regulation of various cancers by playing as a facilitator. Our previous study demonstrated that POU2F2 is highly expressed and accelerates cell proliferation and motility in lung cancer. However, the additional regulatory functions of POU2F2 in LUAD progression require further investigations. In this study, we first confirmed through the UALCAN (A Portal for Facilitating Tumor Subgroup Gene Expression and Survival Analyses) online database that POU2F2 expression is elevated in LUAD tissues. Furthermore, we found that POU2F2 expression is up-regulated in LUAD cell lines. Functional experiments revealed that POU2F2 accelerates LUAD cell proliferation and enhances autophagy through increasing the LC3-II/LC3-I level and fluorescence intensity. Additionally, we discovered that POU2F2 activates the phosphoinositide dependent protein kinase 1 (PDPK1)-mediated phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT) pathway. In conclusion, our discovery firstly disclose that POU2F2 exacerbates cell proliferation and autophagy in LUAD by modulating the PI3K/AKT pathway. This work suggests that POU2F2 may be a hopeful bio-marker for treating LUAD.","PeriodicalId":52382,"journal":{"name":"International Journal of Men''s Social and Community Health","volume":"20 7","pages":"96-96"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147913620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Euodia rutaecarpa fruit attenuates testosterone-induced benign prostatic hyperplasia in rats by inhibiting 5α-reductase activity and androgen receptor signaling pathway","authors":"Yung Hyun Choi","doi":"10.22514/jomh.2024.183","DOIUrl":"https://doi.org/10.22514/jomh.2024.183","url":null,"abstract":"In this study, effect of an ethanol extract of Euodia rutaecarpa fruit (EER), known to have various pharmacological effects, on benign prostatic hyperplasia (BPH) was evaluated. To induce BPH in an in vivo animal model, testosterone propionate (TP) was injected to rats. EER was administered orally with TP injection. Finasteride, a 5α-reductase inhibitor, was used as a positive control. After all mice were sacrificed at the end of the experiment, pathological changes in prostate tissues and levels of key biomarkers involved in BPH development were assessed. Oral administration of EER significantly suppressed TP-induced BPH by diminishing prostate weight, lumen size and epithelial thickness. EER also abrogated the expression of prostate-specific antigen, proliferating cell nuclear antigen, and 5α-reductase type 2 induced by TP. In addition, serum levels of testosterone, dihydrotestosterone (DHT) and prostate specific antigen were elevated in TP challenged rats but decreased in EER-administered rats. Moreover, the improvement effect of EER on TP-induced BPH was associated with decreased expression of androgen receptor (AR) and its coactivators. The current findings show that EER can protect against BPH by attenuating the activation of 5α-reductase and inhibiting the AR signaling pathway, suggesting that EER has great potential in blocking BPH pathogenesis.","PeriodicalId":52382,"journal":{"name":"International Journal of Men''s Social and Community Health","volume":"20 11","pages":"28-28"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147890188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Luteoloside inhibiting the prostate cancer cells growth and promoting the tumor cells autophagy through AKT/mTOR pathway","authors":"Haoyue Li, Xi Wang, Aiyangzi Lu, Yongmei Pan, Wei Zhang, Lei Hao","doi":"10.22514/jomh.2023.047","DOIUrl":"https://doi.org/10.22514/jomh.2023.047","url":null,"abstract":"Prostate cancer (PC) is one of the prevalent tumors in men causing higher mortality. Luteoloside has been discovered for suppressive role into the progression of some cancers. However, the Luteoloside’s regulatory functions regarding PC progression are not well understood. This study is thus designed to investigate the Luteoloside impact on PC progression. In this work, it was demonstrated that the PC cell proliferation was gradually inhibited with the increasing Luteoloside dose (0, 20, 40, 80 µM). Luteoloside also enhanced the PC cell apoptosis. It promoted the autophagy in PC through increasing microtubule-associated protein light chain (LC) 3II/LC3I levels and decreasing p62 levels. Moreover, the Luteoloside reduced phosphorylated-protein kinase B (p-AKT)/AKT and phosphorylated-mechanistic target of rapamycin (p-mTOR)/mTOR levels, indicating that it retarded the AKT/mTOR pathway. In conclusion, the Luteoloside inhibited PC cells growth and promoted tumor cells autophagy through AKT/mTOR pathway. This discovery suggested the Luteoloside as a potential drug in treating PC.","PeriodicalId":52382,"journal":{"name":"International Journal of Men''s Social and Community Health","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://oss.jomh.org/files/article/20230630-37/pdf/JOMH2023040601.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147918265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of GBP5 alleviates lipid accumulation and inflammation in alcoholic fatty liver through inhibition of NF-κB pathway in mice","authors":"Jiangyun Ma, Jian Huang, Xing Wei","doi":"10.22514/jomh.2023.038","DOIUrl":"https://doi.org/10.22514/jomh.2023.038","url":null,"abstract":"Alcoholic liver disease (ALD) is a global liver disease that manifests in a variety of forms, including alcoholic hepatitis, liver inflammation, fatty liver, and liver cirrhosis. One of the early stages of ALD is alcoholic fatty liver (AFL) disease, which is primarily characterized by the accumulation of lipids and inflammation in hepatocytes. Guanylate binding protein 5 (GBP5) has been investigated for its involvement in disease progression. The regulatory effects of GBP5 on the progression of AFL disease are still not well understood. This study aims to investigate the impact of GBP5 on AFL progression and its underlying mechanism of action. To achieve this, gene expression was evaluated using western blot and reverse transcription quantitative polymerase chain reaction (RT-qPCR) methods. Lipid accumulation was confirmed using the Oil Red O staining assay, while the levels of Triglyceride (TG), aspartate aminotransferases (AST), and alanine aminotransferases (ALT) were measured using commercial kits. The levels of inflammatory cytokines were assessed using enzyme-linked immuno sorbent assay (ELISA) assay. Finally, cell apoptosis was evaluated using flow cytometry. Cell apoptosis was evaluated through flow cytometry. Our work demonstrated that GBP5 expression was up-regulated in the Ethyl Alcohol (EtOH) group. Additionally, lipid accumulation was increased after EtOH inducement, but this change was attenuated by silencing GBP5. Silencing of GBP5 reduced EtOH-mediated inflammation and cell apoptosis. Finally, it was discovered that knockdown of GBP5 retarded the EtOH-stimulated nuclear factor kappa-B (NF-κB) pathway. Knockdown of GBP5 alleviated lipid accumulation and inflammation in AFL through inhibition of NF-κB pathway. This finding suggested that GBP5 may be a useful bio-target for AFL treatment.","PeriodicalId":52382,"journal":{"name":"International Journal of Men''s Social and Community Health","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://oss.jomh.org/files/article/20230530-23/pdf/JOMH2023030101.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147918038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Intersectional Mixed Methods Approach to Understand American Indian Men's Health.","authors":"Ka'imi Sinclair,&nbsp;Kelly Gonzales,&nbsp;Claire Woosley,&nbsp;Tish Rivera Cree,&nbsp;Celina M Garza,&nbsp;Dedra Buchwald","doi":"10.22374/ijmsch.v3i2.35","DOIUrl":"10.22374/ijmsch.v3i2.35","url":null,"abstract":"<p><p>This study used a parallel convergent mixed methods design with TribalCrit theory and intersectionality as analytical frameworks to identify how American Indian men's identities intersect with broader structures and systems to shape their eating and physical activity choices and behaviors, and to elicit recommendations for a men's lifestyle intervention. AI men were recruited in Minneapolis, Minnesota and Portland, Oregon between March and December 2017 and in Phoenix, Arizona in December 2019 to participate in a survey and focus groups. The survey included demographic questions and questions about physical and cultural activities men engage in, perceived social support for lifestyle behaviors, masculine characteristics, and values important to American Indian men. The 6-item Kessler Psychological Distress Scale was used to assess psychological distress. Focus groups were audio recorded and transcribed for a phenomenological analysis. Descriptive statistics and correlations were computed for survey data. We conducted 15 focus groups with 151 adult American Indian men in three urban sites. The mean age of participants ranged from 36-51 across the sites; 7%-32% were college graduates; 13%-22% were currently married and 28%-41% were working full time. The most important values reported by participants were being: strong mentally and emotionally, a good parent, responsible, spiritual, and a good spouse or partner. On the K6 psychological distress scale, 63%-70% scored ≥5 but <13 (moderate mental distress), and 8%-15% scored ≥13 indicating severe mental distress. Younger age was significantly correlated with higher mean K6 score (p < .0001). Colonizers and missionaries that settled in the U.S. imposed cultural and gender hegemony which enforced a patriarchal capitalist system that have had long-lasting and deleterious effects on American Indians, particularly American Indian men.</p>","PeriodicalId":52382,"journal":{"name":"International Journal of Men''s Social and Community Health","volume":"3 2","pages":"e66-e89"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8415758/pdf/nihms-1727577.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39387475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}