Qianliening Capsule Promotes Mitochondrial Pathway Mediated the Apoptosis of Benign Prostatic Hyperplasia Epithelial-1 Cells by Regulating the miRNA-181a
Author(s) -
Jianheng Zhou,
Xiaoyong Zhong,
Jiumao Lin,
Zhenfeng Hong
Publication year - 2018
Publication title -
international journal of gerontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.284
H-Index - 16
eISSN - 1873-9598
pISSN - 1873-958X
DOI - 10.1016/j.ijge.2018.04.002
Subject(s) - apoptosis , cytochrome c , flow cytometry , fragmentation (computing) , viability assay , microbiology and biotechnology , dna fragmentation , hyperplasia , medicine , cancer research , pathology , chemistry , biology , programmed cell death , biochemistry , ecology
Summary Background Our previous studies reported that Qianliening capsule (QC) has a significant therapeutic effect on BPH. Therefore, we investigated the effect QC on apoptosis of human prostatic hyperplasia epithelial-1 cells (BPH-1). Methods The BPH-1 cells were treated with various concentrations of QC in vitro. Morphology of BPH-1 cell was observed, and the cell viability was determined by the 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay. The levels of Cytochrome C, caspase-9 and caspase-3 were detected using the flow cytometry and colorimetric assay respectively. The Bax mRNA and the miRNA-221, -222, -15a, -16, -181a was determine by Real-time PCR analysis. Results The apoptosis of BPH-1 cells treated with QC increased than that of untreated cells, as evidenced by loss of plasma membrane asymmetry, the nuclear condensation and fragmentation, collapse of mitochondrial membrane potential in a dose depended manner. The levels of Cytochrome C and caspase-9, caspase-3 in the cells treated with QC increased using the flow cytometry and colorimetric assay respectively. The mRNA and protein expression of Bax and the expression of miRNA-181a in the cells treated with QC increased in a dose dependent manner. Conclusion QC could induce BPH-1 cells apoptosis by regulating miRNA-181a mediated mitochondrial dependent apoptosis pathway, which may be one of the important mechanisms that QC treated benign prostatic hyperplasia.
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