摘要：良性前列腺增生是当前中老年男性发病率最高的良性疾病之一，传统认为雄激素和年龄在其形成过程中发 挥着最主要的作用。目前临床上的主要治疗药物是 2型 5-α还原酶抑制剂 （5α- reductase inhibitors, 5-ARIs）， 但是部分患者治疗无效或逐渐出现药物抵抗，机制不明。大量研究表明，其他性激素如雌激素、孕激素、缩宫素 等，通过作用于其相对应的受体在影响前列腺上皮细胞和间质细胞增殖中也发挥着重要作用。

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[1] CHANG WH, TSAI YS, WANG JY, et al. Sex hormones and oxidative stress mediated phthalate- induced effects in prostatic enlargement [J]. Environ Int, 2019,126: 184-192

[2] CANNARELLA R, CONDORELLI RA, BARBAGALLO F, et al. Endocrinology of the Aging Prostate: Current Concepts [J]. Front Endocrinol, 2021,12:554078

[3] TONG Y, ZHOU RY. Review of the Roles and Interaction of Androgen and Inflammation in Benign Prostatic Hyperplasia [J]. Mediators Inflamm, 2020,2020:7958316

[4] XUE B, WU S, SHARKEY C, et al. Obesity- associated inflammation induces androgenic to estrogenic switch in the prostate gland [J]. Prostate Cancer Prostatic Dis, 2020,23 (3):465-474

[5] CHOI YJ, FAN M, TANG Y, et al. In Vivo Effects of Polymerized Anthocyanin from Grape Skin on Benign Prostatic Hyperplasia [J]. Nutrients, 2019,14;11(10):2444

[6] KIM Y, LEE D, JO H, et al. GV1001 interacts with androgen receptor to inhibit prostate cell proliferation in benign prostatic hyperplasia by regulating expression of molecules related to epithelial- mesenchymal transition [J]. Aging, 2021,13(3):3202-3217

[7] LIU D, SHOAG JE, POLIAK D, et al. Integrative multiplatform molecular profiling of benign prostatic hyperplasia identifies distinct subtypes [J]. Nat Commun, 2020,11 (1):1987

[8] ZHANG B, KWON OJ, HENRY G, et al. Non- Cell- Autonomous Regulation of Prostate Epithelial Homeostasis by Androgen Receptor [J]. Mol Cell, 2016,63(6):976-989

[9] LIN ZM, FAN DD, JIN S, et al. Methylated CpG dinucleotides in the 5-α reductase 2 gene may explain finasteride resistance in benign prostatic enlargement patients [J]. Asian J Androl, 2021,23(3):266-272

[10] JIANG CY, YANG BY, ZHAO S, et al. Deregulation of ATG9A by impaired AR signaling induces autophagy in prostate stromal fibroblasts and promotes BPH progression [J]. Cell Death Dis, 2018,9(4):431

[11] YANG BY, JIANG CY, DAI CY, et al. 5- ARI induces autophagy of prostate epithelial cells through suppressing IGF- 1 expression in prostate fibroblasts [J]. Cell Prolif, 2019,52(3):e12590

[12] 朱自强,康健.良性前列腺增生最新研究进展[J].临床泌尿外科杂 志,2019,34(05):409-412

[13] QU LG, WARDAN H, DAVIS ID, et al. Effects of estrogen receptor signaling on prostate cancer carcinogenesis [J]. Transl Res, 2020,222:56-66

[14] FAN Y, SONG TR, WEI Q, et al. Modulatory effect of aquaporin 5 on estrogen- induced epithelial- mesenchymal transition in prostate epithelial cells [J]. Chin Med J, 2020, 134(4):448-455

[15] SHI X, PENG Y, DU X, et al. Estradiol promotes epithelial- to-mesenchymal transition in human benign prostatic epithelial cells [J]. Prostate, 2017,77(14):1424-1437

[16] MIAO L, JIAO C, SHAO R, et al. Bakuchiol suppresses oestrogen/testosterone- induced Benign Prostatic Hyperplasia development through up- regulation of epithelial estrogen receptor β and down- regulation of stromal aromatase [J]. Toxicol Appl Pharmacol, 2019,381:114637

[17] NICHOLSON TM, MOSES MA, UCHTMANN KS, et al. Estrogen receptor-α is a key mediator and therapeutic target for bladder complications of benign prostatic hyperplasia [J]. J Urol, 2015,193(2):722-729

[18] HERNÁNDEZ- SILVA CD, VILLEGAS- PINEDA JC, PEREIRA- SUÁREZ AL. Expression and Role of the G Protein- Coupled Estrogen Receptor (GPR30/GPER) in the Development and Immune Response in Female Reproductive Cancers [J]. Front Endocrinol (Lausanne), 2020,11:544

[19] RAGO V, ROMEO F, GIORDANO F, et al. Identification of the G protein- coupled estrogen receptor (GPER) in human prostate: expression site of the estrogen receptor in the benign and neoplastic gland [J]. Andrology, 2016,4(1): 121-127

[20] COMEGLIO P, MORELLI A, CELLAI I, et al. Opposite effects of tamoxifen on metabolic syndrome- induced bladder and prostate alterations: a role for GPR30/GPER? [J]. Prostate, 2014,74(1):10-28

[21] YANG DL, XU JW, ZHU JG, et al. Role of GPR30 in estrogen- induced prostate epithelial apoptosis and benign prostatic hyperplasia [J]. BMC Health Serv Res, 2017,487 (3):517-524

[22] 董卫民,卢剑铭,朱建国,等.GPER的激活调控自噬抑制前列腺上 皮细胞增殖[J].中华医学杂志,2019,6:419-422

[23] WANG Z, HU L, SALARI K, et al. Androgenic to oestrogenic switch in the human adult prostate gland is regulated by epigenetic silencing of steroid 5α- reductase 2 [J]. J Pathol, 2017,243(4):457-467

[24] CHEN R, YU Y, DONG X. Progesterone receptor in the prostate: A potential suppressor for benign prostatic hyperplasia and prostate cancer [J]. J Steroid Biochem Mol Biol, 2017,166:91-96

[25] ASAVASUPREECHAR T, SAITO R, MIKI Y, et al. Systemic distribution of progesterone receptor subtypes in human tissues [J]. J Steroid Biochem Mol Biol, 2020,199: 105599

[26] YU Y, LIU L, XIE N, et al. Expression and function of the progesterone receptor in human prostate stroma provide novel insights to cell proliferation control [J]. J Clin Endocrinol Metab, 2013,98(7):2887-2896

[27] SONG L, SHEN W, ZHANG H, et al. Differential expression of androgen, estrogen, and progesterone receptors in benign prostatic hyperplasia [J]. Bosn J Basic Med Sci, 2016,16(3):201-208

[28] XU Z, MA T, ZHOU J, et al. Nuclear receptor ERRα contributes to castration- resistant growth of prostate cancer via its regulation of intratumoral androgen biosynthesis [J]. Theranostics, 2020,10(9):4201-4216

[29] STADLER B, WHITTAKER MR, EXINTARIS B, et al. Oxytocin in the Male Reproductive Tract; The Therapeutic Potential of Oxytocin- Agonists and- Antagonists [J]. Front Endocrinol (Lausanne), 2020,11:565731

[30] ASSINDER SJ. Oxytocin increases 5alpha- reductase activity of human prostate epithelial cells, but not stromal cells [J]. Prostate, 2008,68(2):115-121

[31] LI Z, XIAO H, WANG K, et al. Upregulation of Oxytocin Receptor in the Hyperplastic Prostate [J]. Front Endocrinol (Lausanne), 2018,9:403

[32] XU H, FU S, CHEN Y, et al. Oxytocin: its role in benign prostatic hyperplasia via the ERK pathway [J]. Clin Sci (Lond), 2017,131(7):595-607

[33] GOULD ML, NICHOLSON HD. Changes in receptor location affect the ability of oxytocin to stimulate proliferative growth in prostate epithelial cells [J]. Reprod Fertil Dev, 2019,31(6):1166-1179

[34] LEE SN, KRASKA J, PAPARGIRIS M, et al. Oxytocin receptor antagonists as a novel pharmacological agent for reducing smooth muscle tone in the human prostate [J]. Sci Rep, 2021,11(1):6352

[35] BERIO E, DIVARI S, STARVAGGI CUCUZZA L, et al. 17- estradiol upregulates oxytocin and the oxytocin receptor in C2C12 myotubes [J]. Peer J, 2017,5:e3124. 

刘占良,牛亦农. 性激素与良性前列腺增生关系的研究进展[J]. 泌尿外科杂志（电子版）,2021,13(2):96-99. DOI:10.3969/j.issn.1674-7410.2021.02.021.

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良性前列腺增生 （benign prostatic hyperplasia, BPH） 是影响中老年男性生活质量最常见的疾病之一， 会导致良性前列腺增大 （benign prostatic enlargement, BPE）、良性前列腺梗阻（benign prostatic obstruction, BPO） 和 下 尿 路 梗 阻 症 状 （lower urinary tract symptoms, LUTS） [1] 。BPH的发病率随 着年龄的增长不断升高，其患病率在40岁的男性中约 为5%~10%，而在70~80岁的男性中则达到80%[2] 。 

前列腺是激素敏感的器官[1] ，传统认为雄激素在 BPH形成过程中发挥着最主要的作用，2型5α还原酶 抑制剂 （5 α- reductase inhibitors, 5-ARIs） 通过阻 断体内的睾酮 （testosterone, T） 向双氢睾酮 （dihydrotestosterone, DHT） 转化，削弱雄激素相关信 号通路，诱导前列腺上皮细胞凋亡，缩小前列腺体 积，缓解下尿路症状，是目前临床上治疗 BPH 的一 线用药[3] 。但是在接受 5- ARIs治疗的 BPH 患者中， 至少有 30%的患者临床症状没有改善，甚至出现疾 病进展[4] 。因此探索BPH形成原因及部分BPH患者5- ARIs治疗失败和疾病进展的机制具有重要意义。 

BPH 的具体发生机制目前仍不明确，除了雄激 素外，多种性激素如雌激素、孕激素、缩宫素等都 可能在 BPH 的发生发展中起到重要的作用，本文就 BPH与性激素的关系及其相关研究进展综述如下。

1 雄激素与前列腺增生

2 雌激素与前列腺增生

3 孕激素与前列腺增生

4 缩宫素与前列腺增生

5 结语与展望

5 结语与展望 

前列腺是一个激素敏感的器官，除雄激素是 BPH 形成、发展的必要激素外，多种性激素如雌激 素、孕激素、缩宫素等在 BPH 的形成和发展中也都 起到了重要的作用。如前所述，对 5-ARIs发生抵抗 的 BPH 患者，可能由于 SRD5A2基因的启动子发生 甲基化，前列腺内 DHT 合成减少、T 堆积，T 在芳 香化酶的催化下转化成雌激素，雌激素通过作用于 雌激素受体促进 BPH 进展，与此同时孕激素、缩宫 素可能协同雌激素发挥作用。虽然部分研究已经描 述了这些激素对 BPH 的影响，但还没有得出关于它 们在疾病进展中如何作用以及激素之间相互作用的 结论，未来还需要更多相关研究进一步探讨性激素 与 BPH的关系，完善 BPH的临床治疗方案。

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