Abstract
This study aimed to investigate the beneficial effects of A. melanocarpa on testosterone propionate (TP)-induced benign prostatic hyperplasia (BPH) in Wistar rats. Moreover, the bioactive constituents in the extract were determined using LC/MS and HPLC analyses. The dried fruits of A. melanocarpa were extracted using accelerated solvent extraction (ASE) under different extract conditions (temperature, 30 °C or 100 °C; extract solvent, 60% or 100% ethanol) to yield four extracts (T1~T4). Of the four A. melanocarpa extracts, T1 extracted under the condition of 100% ethanol/low temperature (30 °C) exhibited the greatest inhibitory activity on TP-induced prostatic hyperplasia in rats. The administration of T1 (100 mg/kg body weight, p.o.) for six weeks attenuated TP-induced prostate enlargement and reduced the levels of dihydrotestosterone (DHT) and 5α-reductase in both serum and prostate tissue. The suppression of PCNA mRNA expression in prostate tissue was remarkable in T1-treated rats. In LC/MS analysis, the levels of main anthocyanins and phenolics were significantly higher in T1 than in the other extracts. Furthermore, the quantitative study showed that the contents of cyanidin-3-glucose and cyanidin-3-xylose in T1 exhibited 1.27~1.67 and 1.10~1.26 folds higher compared to those in the other extracts. These findings demonstrated that A. melanocarpa extract containing anthocyanins as bioactive constituents attenuated the development of testosterone-induced prostatic hyperplasia, and suggested that this extract has therapeutic potential to treat prostate enlargement and BPH.
Highlights
Benign prostatic hyperplasia (BPH) is a pathologic process that is more likely to develop after middle age [1]
Effects of A. melanocarpa Extracts on Prostate Index (PI) and Serum Liver Enzymes in the testosterone propionate (TP)-Induced BPH Murine Model
Six weeks after the induction of BPH by TP injection and the co-treatment of test samples into seven-week-old Wistar rats, it was found that the absolute prostate weight and PI was considerably increased as compared to non-TP-treated controls (Sham group) (Figure 1)
Summary
Benign prostatic hyperplasia (BPH) is a pathologic process that is more likely to develop after middle age [1]. The precise mechanism responsible for the development of hyperplasia has not been definitively established, but sex hormones, stromal-epithelial interaction, growth hormones, and neurotransmitters acting in concert may result in abnormal cell death or apoptosis or the excessive proliferation of epithelial and stromal cells which give to the pathogenesis of BPH [5,6]. The therapeutic effects of 5α-reductase inhibitors, such as finasteride and dutasteride, on prostate hyperplasia have been firmly established, and their adverse event profiles make them suitable for long-term use [11,12]
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