Aerobic exercise ameliorates benign prostatic hyperplasia in obese mice through downregulating the AR/androgen/PI3K/AKT signaling pathway.

Abstract

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.