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雄激素是否调节炎症的病理生理途径?评估当代证据。

Do Androgens Modulate the Pathophysiological Pathways of Inflammation? Appraising the Contemporary Evidence.

作者信息

Traish Abdulmaged, Bolanos Jose, Nair Sunil, Saad Farid, Morgentaler Abraham

机构信息

Department of Urology, Boston University School of Medicine, Boston, MA 02118, USA.

Men's Health Boston, Chestnut Hill, MA 02467, USA.

出版信息

J Clin Med. 2018 Dec 14;7(12):549. doi: 10.3390/jcm7120549.

DOI:10.3390/jcm7120549
PMID:30558178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6306858/
Abstract

The role of testosterone in the pathophysiology of inflammation is of critical clinical importance; however, no universal mechanism(s) has been advanced to explain the complex and interwoven pathways of androgens in the attenuation of the inflammatory processes. PubMed and EMBASE searches were performed, including the following key words: "testosterone", "androgens", "inflammatory cytokines", "inflammatory biomarkers" with focus on clinical studies as well as basic scientific studies in human and animal models. Significant benefits of testosterone therapy in ameliorating or attenuating the symptoms of several chronic inflammatory diseases were reported. Because anti⁻tumor necrosis factor therapy is the mainstay for the treatment of moderate-to-severe inflammatory bowel disease; including Crohn's disease and ulcerative colitis, and because testosterone therapy in hypogonadal men with chronic inflammatory conditions reduce tumor necrosis factor-alpha (TNF-α), IL-1β, and IL-6, we suggest that testosterone therapy attenuates the inflammatory process and reduces the burden of disease by mechanisms inhibiting inflammatory cytokine expression and function. Mechanistically, androgens regulate the expression and function of inflammatory cytokines, including TNF-α, IL-1β, IL-6, and CRP (C-reactive protein). Here, we suggest that testosterone regulates multiple and overlapping cellular and molecular pathways involving a host of immune cells and biochemical factors that converge to contribute to attenuation of the inflammatory process.

摘要

睾酮在炎症病理生理学中的作用具有至关重要的临床意义;然而,尚未提出通用机制来解释雄激素在减轻炎症过程中复杂且相互交织的途径。我们进行了PubMed和EMBASE检索,包括以下关键词:“睾酮”、“雄激素”、“炎性细胞因子”、“炎症生物标志物”,重点关注临床研究以及人类和动物模型的基础科学研究。有报道称,睾酮治疗在改善或减轻几种慢性炎症性疾病症状方面具有显著益处。由于抗肿瘤坏死因子治疗是中重度炎症性肠病(包括克罗恩病和溃疡性结肠炎)治疗的主要手段,且由于睾酮治疗可降低患有慢性炎症性疾病的性腺功能减退男性体内的肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)水平,我们认为睾酮治疗通过抑制炎性细胞因子表达和功能的机制减轻炎症过程并降低疾病负担。从机制上讲,雄激素可调节炎性细胞因子的表达和功能,包括TNF-α、IL-1β、IL-6和C反应蛋白(CRP)。在此,我们认为睾酮可调节涉及众多免疫细胞和生化因子的多种且相互重叠的细胞和分子途径,这些途径共同作用有助于减轻炎症过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d1/6306858/e04b273d1cc1/jcm-07-00549-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d1/6306858/361ec1816712/jcm-07-00549-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d1/6306858/e04b273d1cc1/jcm-07-00549-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d1/6306858/361ec1816712/jcm-07-00549-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d1/6306858/e04b273d1cc1/jcm-07-00549-g002.jpg

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