Medical College, Guizhou University, Guiyang, 550025, Guizhou, China.
Department of Urology Surgery, Guizhou Province People's Hospital, Guiyang, 550002, China.
Mol Cell Biochem. 2023 Dec;478(12):2721-2737. doi: 10.1007/s11010-023-04695-2. Epub 2023 Mar 15.
In ageing men, benign prostatic hyperplasia (BPH) is a chronic disease that leads to progressive lower urinary tract symptoms (LUTS) caused by obstruction of the bladder outlet (BOO). Patients with LUTS (such as increased frequency and urgency of urination) and complications of BOO (such as hydronephrosis and bladder stones) are at risk of serious health problems. BPH causes a rapidly rising burden of LUTS far exceeding that of other urological conditions. Treatment outcomes are unsatisfactory for BPH largely due to the lacking of fully understanding of the pathogenesis. Hormonal imbalances related to androgen and oestrogen can cause BPH, but the exact mechanism is still unknown, even the animal model is not fully understood. Additionally, there are no large-scale data to explain this mechanism. A BPH mouse model was established using mixed slow-release pellets of testosterone (T) and estradiol (E2), and we measured gene expression in mouse prostate tissue using RNA-seq, verified the results using qRT‒PCR, and used bioinformatics methods to analyse the differentially expressed genes (DEGs).
在老年男性中,良性前列腺增生(BPH)是一种慢性疾病,会导致膀胱出口梗阻(BOO)引起的下尿路症状(LUTS)逐渐加重。有 LUTS(如尿频和尿急增加)和 BOO 并发症(如肾积水和膀胱结石)的患者存在严重健康问题的风险。BPH 导致的 LUTS 负担迅速上升,远远超过其他泌尿科疾病。BPH 的治疗效果不尽如人意,主要是因为对发病机制的了解不足。与雄激素和雌激素相关的激素失衡可能导致 BPH,但确切的机制仍不清楚,甚至动物模型也不完全了解。此外,没有大规模的数据来解释这种机制。我们使用混合的睾酮(T)和雌二醇(E2)缓释微球建立了 BPH 小鼠模型,并使用 RNA-seq 测量了小鼠前列腺组织中的基因表达,使用 qRT-PCR 验证了结果,并使用生物信息学方法分析了差异表达基因(DEGs)。