Qianliening capsule (前列宁胶囊) inhibits human prostate cell growth via induction of mitochondrion-dependent cell apoptosis.

Autor:	Hong, Zhen-feng, Lin, Jiu-mao, Zhong, Xiao-yong, Li, Ying, Zhou, Jian-heng, Xu, Wei, Peng, Jun
Předmět:	RNA analysis ANALYSIS of variance APOPTOSIS PHARMACEUTICAL encapsulation CELL culture CELL lines COLORIMETRY DOSE-effect relationship in pharmacology HERBAL medicine CHINESE medicine MICROSCOPY MITOCHONDRIA POLYMERASE chain reaction RESEARCH funding STAINS & staining (Microscopy) T-test (Statistics) WESTERN immunoblotting BENIGN prostatic hyperplasia REVERSE transcriptase polymerase chain reaction DATA analysis software IN vitro studies
Zdroj:	Chinese Journal of Integrative Medicine; Nov2012, Vol. 18 Issue 11, p824-830, 7p
Abstrakt:	Objective: To investigate the molecular mechanisms by which Qianliening Capsule (前列宁胶囊, QC) treats benign prostatic hyperplasia (BPH). Methods: Human prostate stromal cell line WPMY-1 was treated with 0, 1, 3 and 5 mg/mL of QC for 24, 48 and 72 h, respectively, in the presence of 10 ng/mL basic fibroblast growth factor (bFGF). The viability of WPMY-1 cells was determined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell morphology was observed by phase-contrast microscopy. 4′,6-diamidino-2-phenylindole (DAPI) staining and fluorescence activated cell sorting (FACS) analysis with Annexin-V/propidium iodide (PI) staining were performed to determine cell apoptosis. The loss of mitochondrial membrane potential was examined by FACS analysis with 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolyl-carbocyarine iodide (JC-1) staining. Activation of caspase-3 and -9 was evaluated by colorimetric assay. The mRNA and protein expression levels of Bcl-2 and Bax were measured by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting, respectively. Results: Upon bFGF stimulation, the viability of WPMY-1 cells was increased to 122%-118% compared with the control cells ( P <0.05). However, treatment with 1-5 mg/mL of QC for 24, 48 and 72 h decreased the viability of bFGF-stimulated cells to 80%-92%, 59%-82%, 36%-62% compared with the untreated cells ( P <0.05). In addition, QC treatment reduced WPMY-1 cell density in a dose-dependent manner. Moreover, QC treatment dose-dependently induced the loss of plasma membrane asymmetry, the nuclear condensation and fragmentation, collapse of mitochondrial membrane potential, activation of caspase-9 and caspase-3, and increase of pro-apoptotic Bax/Bcl-2 ratio. Conclusion: Promoting mitochondrion-dependent apoptosis of prostate stromal cells might be one of the mechanisms by which QC treats BPH. [ABSTRACT FROM AUTHOR]
Databáze:	Complementary Index
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