MOLECULAR MECHANISMS OF NOCICEPTION IN CHRONIC PROSTATITIS

I. Gorpynchenko, Kamil R. Nurimanov, Olena Nedogonova
{"title":"MOLECULAR MECHANISMS OF NOCICEPTION IN CHRONIC PROSTATITIS","authors":"I. Gorpynchenko, Kamil R. Nurimanov, Olena Nedogonova","doi":"10.31612/2616-4868.8.2023.15","DOIUrl":null,"url":null,"abstract":"Introduction. The need to understand the pathophysiology of prostatitis is determined by its prevalence, usually chronic progressive course, significant impact on quality of life, fertility and sexuality. The modern arsenal of medicines allows us to achieve a clinically significant effect. Along with this, non-pharmacological methods are widely used to increase the effectiveness of treatment. However, despite significant successes in the treatment of prostatitis, the problems of insufficient efficiency remain unsolved by modern urology, and it is extremely difficult to help these patients. Understanding the pathophysiology of the disease has always been the key to successful diagnosis and treatment. That is why it is important to determine the mechanisms of development of painful manifestations of prostatitis. The aim. To describe the main molecular mechanisms of tissue damage reception, in particular of the prostate gland, which are perceived as pain sensations. Materials and methods. An evaluation of modern literature devoted to the mechanisms of creation of nerve impulses due to damage and inflammation of the prostate gland was carried out. The search was conducted in the MEDLINE and databases of the National Library of Ukraine named after V.I. Vernadsky. Results. The main molecular mechanisms of nociception in chronic prostatitis have been determined. A review of modern literature devoted to the study of pain mechanisms as a biologically significant signal of damage at the molecular level of reception is presented. Attention is focused on the features of nociception in prostatitis, its connection with the production of inflammatory mediators, possible mechanisms of hyperalgesia and allodynia. As a result of stress and tissue damage, the production and release of inflammatory mediators such as interleukins, interferon, prostaglandins, bradykinin, adenosine triphosphate, protons and nerve growth factor increase. These mediators activate pain receptors located on nerve endings and are ion channels of various types: transient receptor potential, acid, purinergic, and potassium ion leak channels. Conclusions. The presented literature data describe the mechanisms of nociception, hyperalgesia and allodynia in chronic prostatitis, the understanding of which can be the basis for the development of new methods of diagnosis and treatment.","PeriodicalId":502404,"journal":{"name":"Clinical and Preventive Medicine","volume":"35 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and Preventive Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.31612/2616-4868.8.2023.15","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction. The need to understand the pathophysiology of prostatitis is determined by its prevalence, usually chronic progressive course, significant impact on quality of life, fertility and sexuality. The modern arsenal of medicines allows us to achieve a clinically significant effect. Along with this, non-pharmacological methods are widely used to increase the effectiveness of treatment. However, despite significant successes in the treatment of prostatitis, the problems of insufficient efficiency remain unsolved by modern urology, and it is extremely difficult to help these patients. Understanding the pathophysiology of the disease has always been the key to successful diagnosis and treatment. That is why it is important to determine the mechanisms of development of painful manifestations of prostatitis. The aim. To describe the main molecular mechanisms of tissue damage reception, in particular of the prostate gland, which are perceived as pain sensations. Materials and methods. An evaluation of modern literature devoted to the mechanisms of creation of nerve impulses due to damage and inflammation of the prostate gland was carried out. The search was conducted in the MEDLINE and databases of the National Library of Ukraine named after V.I. Vernadsky. Results. The main molecular mechanisms of nociception in chronic prostatitis have been determined. A review of modern literature devoted to the study of pain mechanisms as a biologically significant signal of damage at the molecular level of reception is presented. Attention is focused on the features of nociception in prostatitis, its connection with the production of inflammatory mediators, possible mechanisms of hyperalgesia and allodynia. As a result of stress and tissue damage, the production and release of inflammatory mediators such as interleukins, interferon, prostaglandins, bradykinin, adenosine triphosphate, protons and nerve growth factor increase. These mediators activate pain receptors located on nerve endings and are ion channels of various types: transient receptor potential, acid, purinergic, and potassium ion leak channels. Conclusions. The presented literature data describe the mechanisms of nociception, hyperalgesia and allodynia in chronic prostatitis, the understanding of which can be the basis for the development of new methods of diagnosis and treatment.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
慢性前列腺炎痛觉的分子机制
前言。前列腺炎发病率高,病程通常呈慢性进行性发展,对生活质量、生育能力和性生活有重大影响,因此有必要了解前列腺炎的病理生理学。现代药物库使我们能够取得显著的临床疗效。与此同时,非药物治疗方法也被广泛用于提高治疗效果。然而,尽管在治疗前列腺炎方面取得了重大成就,但现代泌尿外科仍无法解决疗效不佳的问题,要帮助这些患者极其困难。了解疾病的病理生理学一直是成功诊断和治疗的关键。因此,确定前列腺炎疼痛表现的发生机制非常重要。 我们的目标是描述组织损伤接收的主要分子机制,尤其是前列腺组织损伤接收的主要分子机制。 材料和方法。对有关前列腺损伤和炎症导致神经冲动产生机制的现代文献进行了评估。在 MEDLINE 和以 V.I. Vernadsky 命名的乌克兰国家图书馆数据库中进行了搜索。 研究结果确定了慢性前列腺炎痛觉的主要分子机制。本文对专门研究疼痛机制的现代文献进行了综述,疼痛机制是一种在分子接收水平上具有生物学意义的损伤信号。重点关注前列腺炎的痛觉特征、其与炎症介质产生的联系、痛觉减退和异动症的可能机制。 由于压力和组织损伤,白细胞介素、干扰素、前列腺素、缓激肽、三磷酸腺苷、质子和神经生长因子等炎症介质的产生和释放增加。这些介质会激活位于神经末梢的痛觉受体,它们是各种类型的离子通道:瞬时受体电位通道、酸通道、嘌呤能通道和钾离子泄漏通道。 结论。所提供的文献资料描述了慢性前列腺炎的痛觉、痛觉减退和异动症的机制,对这些机制的了解可作为开发新的诊断和治疗方法的基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
IMPROVEMENT OF INSTRUMENTAL DIAGNOSTICS OF NODAL PATHOLOGY OF THE THYROID GLAND ANTIMICROBIAL ACTIVITY ASSESSMENT OF FOOD PRESERVATIVES CONTAINING ORGANIC CARBOXYLIC ACIDS JUSTIFICATION OF APPROACHES TO THE ORGANIZATION OF REHABILITATION OF PATIENTS WITH UROLITHIASIS ASSESSMENT OF THE RISKS OF MALIGNANT NEOPLASMS IN THE POPULATION WHEN REUSING MINE WATER ENHANCED MODEL OF THE SYSTEM FOR PROVIDING COSMETOLOGY SERVICES TO THE POPULATION
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1