Qianliening capsules influence the apoptosis of benign prostatic hyperplasia epithelial-1 cells by regulating the extracellular matrix

Abstract

The present study investigated whether Qianliening capsules (QC) affected the apoptosis of benign prostatic hyperplastia epithelial (BPH‑1) cells by regulating the extracellular matrix (ECM). The levels of fibronectin (FN) and collagen IV were determined in the culture medium of BPH‑1 cells maintained in normal medium and of BPH‑1 cells maintained in an environment rich in FN and collagen IV using an enzyme‑linked immunosorbent assay. Reverse transcription quantitative polymerase chain reaction and western blot analysis were performed to determine the mRNA and protein expression levels of FN, collagen IV, B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein (Bax) and cyclin D1, respectively. The cell morphology and viability were determined using light microscopy and an MTT assay and cell apoptosis was detected by annexin V staining. The results demonstrated that FN and collagen IV affected the apoptotic response of the BPH‑1 cells, QC treatment significantly reduced the levels of FN and collagen IV secreted by the cells into the culture medium (P<0.01), inhibited the mRNA and protein expression levels of FN, collagen IV, Bcl‑2 and cyclin D1 and promoted the mRNA and protein expression of Bax. Therefore, one of the mechanisms underlying the anti‑BPH action of QC involves promoting apoptosis by regulating the expression of the extracellular matrix.

miRNA Regulation Network Analysis in Qianliening Capsule Treatment of Benign Prostatic Hyperplasia

“…Our preliminary research showed that QC could inhibit proliferation and promoted apoptosis in vivo and in vitro [ 20 , 21 ]. According to our miRNA array results, most of the miRNAs have previously been shown to be associated with apoptosis, proliferation, and metabolism.…”

“…Our preliminary study in a rat model of BPH showed that QC significantly decreased prostatic volume and weight, inhibited prostatic hyperplasia, attenuated abnormal serum levels of estrogen and androgen, regulated the expression of estrogen receptor (ER), androgen receptor (AR), and related mRNA, inhibited the EGF/STAT3 pathway, and reduced expression of proproliferative PCNA, cyclin D1, and CDK4 proteins [ 15 – 19 ]. Moreover, QC effectively inhibited proliferation and promoted apoptosis in human benign prostatic hyperplasia epithelial cells and prostate cells [ 20 , 21 ]. To more fully clarify the mechanistic effects of QC therapy in the treatment of BPH, we performed the present study to examine the effects of QC on expression of specifically expressed miRNAs, genes, and relevant signaling pathways in our rat model of BPH.…”