School of Kinesiology, Shanghai University of Sport, Shanghai, China.
School of Kinesiology, Shanghai University of Sport, Shanghai, China.
Exp Gerontol. 2021 Jan;143:111152. doi: 10.1016/j.exger.2020.111152. Epub 2020 Nov 13.
Emerging evidence has suggested that physical activities can reduce the risk of benign prostatic hyperplasia (BPH). Here, we evaluated the effect of aerobic exercise in a model of BPH using obese mice.
Obese C57BL/6J mice in the control group, obesity group (OB), and obesity group plus exercise (OB + E) with eight weeks training were inspected for morphological alterations via hematoxylin-eosin (H&E) staining, lipid and sex hormone metabolites via enzyme-linked immunosorbent assays (ELISAs), relative protein expression via Western blotting, and prostate cancer-up-regulated long noncoding RNA (PlncRNA) and androgen receptor (AR) mRNA levels via quantitative real-time PCR (qRT-PCR).
Aerobic exercise training slowed fat-mass gain in OB mice. Prostate volume (PV) and area of lumen was significantly decreased in OB mice and was slightly increased following aerobic exercise. Epithelial volume density in the OB group was higher than that in the control group. Furthermore, aerobic exercise lowered serum low-density lipoprotein (LDL), triglyceride, and free fatty acid (FFA) levels, whereas it raised high-density lipoprotein (HDL) levels in OB + E mice. Additionally, the hormonal ratio of estradiol/testosterone (E2/T) approached that of the control group following aerobic exercise in OB + E mice. Mechanistically, aerobic exercise downregulated the PlncRNA-AR/androgen signaling pathway via the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) axis in the prostates of OB + E mice.
These data demonstrate that aerobic exercise may alleviate BPH in obese mice through regulation of the AR/androgen/PI3K/AKT signaling pathway.
越来越多的证据表明，身体活动可以降低良性前列腺增生（BPH）的风险。在这里，我们使用肥胖小鼠评估了有氧运动对 BPH 模型的影响。
通过苏木精-伊红（H&E）染色、酶联免疫吸附测定（ELISA）检测血脂和性激素代谢物、Western blot 检测相对蛋白表达、定量实时 PCR（qRT-PCR）检测前列腺癌上调的长链非编码 RNA（PlncRNA）和雄激素受体（AR）mRNA 水平，观察肥胖 C57BL/6J 小鼠的对照组、肥胖组（OB）和肥胖加运动组（OB+E）的形态学改变，其中肥胖加运动组进行了八周的训练。
有氧运动训练减缓了 OB 小鼠的脂肪量增加。OB 小鼠的前列腺体积（PV）和管腔面积明显减少，有氧运动后略有增加。OB 组的上皮体积密度高于对照组。此外，有氧运动降低了 OB+E 小鼠的血清低密度脂蛋白（LDL）、甘油三酯和游离脂肪酸（FFA）水平，而提高了高密度脂蛋白（HDL）水平。此外，有氧运动使 OB+E 小鼠的雌二醇/睾酮（E2/T）激素比值接近对照组。在机制上，有氧运动通过前列腺中的磷脂酰肌醇 3-激酶/蛋白激酶 B（PI3K/AKT）轴下调 PlncRNA-AR/雄激素信号通路。
这些数据表明，有氧运动可能通过调节 AR/雄激素/PI3K/AKT 信号通路缓解肥胖小鼠的 BPH。
