Abstract：
Benign prostatic hyperplasia, a prevalent condition in aging men, is characterized by the proliferation of prostatic epithelial and stromal cells, which leads to bladder outlet obstruction and the exacerbation of lower urinary tract symptoms. There is increasing evidence that chronic prostatic inflammation contributes to the pathogenesis and progression of benign prostatic hyperplasia. This review explores the complex relationship between chronic inflammation and benign prostatic hyperplasia, focusing on the underlying mechanisms, clinical implications, and current therapeutic approaches. The pathophysiology of benign prostatic hyperplasia is multifaceted, involving factors such as hormonal changes, hypoxia, urine reflux into prostatic ducts and stroma, autoimmune responses, and infection-induced inflammation. Inflammatory cytokines, particularly interleukin-17 and interleukin-8, may play key roles in tissue remodeling and smooth muscle contraction within the prostate, thereby influencing benign prostatic hyperplasia progression. Current therapies for benign prostatic hyperplasia include α1-blockers, phosphodiesterase 5 inhibitors, 5α-reductase inhibitors, and plant-based treatments (e.g., pollen extract). These therapies aim to alleviate symptoms by reducing prostatic inflammation, improving blood flow, and inhibiting hormonal pathways involved in prostatic enlargement. However, patients with chronic prostatic inflammation often experience more severe lower urinary tract symptoms and may be resistant to conventional treatments. This resistance has prompted the exploration of alternative therapies targeting inflammation. Chronic prostatic inflammation plays a central role in the pathogenesis and severity of benign prostatic hyperplasia. An understanding of its mechanisms will enable the development of more effective treatments to improve the quality of life among patients with benign prostatic hyperplasia.
摘要：
良性前列腺增生,老年男性的普遍状况，以前列腺上皮细胞和基质细胞的增殖为特征，导致膀胱出口梗阻和下尿路症状加重。越来越多的证据表明，慢性前列腺炎症有助于良性前列腺增生的发病和进展。本文就慢性炎症与良性前列腺增生的复杂关系作一综述,着眼于潜在的机制，临床意义，和目前的治疗方法。良性前列腺增生的病理生理学是多方面的,包括荷尔蒙变化等因素，缺氧,尿液回流到前列腺导管和间质，自身免疫反应，和感染引起的炎症。炎性细胞因子,特别是白细胞介素-17和白细胞介素-8，可能在前列腺内的组织重塑和平滑肌收缩中起关键作用，从而影响良性前列腺增生的进展。目前良性前列腺增生的治疗包括α1-受体阻滞剂，磷酸二酯酶5抑制剂，5α-还原酶抑制剂，和基于植物的处理(例如，花粉提取物）。这些疗法旨在通过减少前列腺炎症来缓解症状，改善血液流动，并抑制与前列腺增大有关的激素途径。然而,慢性前列腺炎症患者通常会出现更严重的下尿路症状，并且可能对常规治疗产生抗药性。这种耐药性促使人们探索针对炎症的替代疗法。慢性前列腺炎症在良性前列腺增生的发病机制和严重程度中起着重要作用。了解其机制将有助于开发更有效的治疗方法，以改善良性前列腺增生患者的生活质量。
