Qianliening capsule (前列宁胶囊) inhibits human prostate cell growth via induction of mitochondrion-dependent cell apoptosis
Back to article page
OriginalPaper|Updated:2021-08-27
|
Qianliening capsule (前列宁胶囊) inhibits human prostate cell growth via induction of mitochondrion-dependent cell apoptosis
Qianliening capsule (前列宁胶囊) inhibits human prostate cell growth via induction of mitochondrion-dependent cell apoptosis
中国结合医学杂志(英文版)2012年18卷第11期 页码:824-830
Affiliations:
1. Academy of Integrative Medicine Biomedical Research Center, Fujian University of Traditional Chinese Medicine,Fuzhou,China
2. Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine,Fuzhou,China
3. Department of Integrative Medicine, Fujian University of Traditional Chinese Medicine,Fuzhou,China
4. Department of Pharmacology, Fujian University of Traditional Chinese Medicine,Fuzhou,China
Author bio:
Funds:
Supported by the National Natural Science Foundation of China (No. 81072927 and No. 81173433), the Natural Science Foundation of Fujian Province of China (No. 2010J01199 and No. 2009J01169)
Hong, Zf., Lin, Jm., Zhong, Xy. et al. Qianliening capsule (前列宁胶囊) inhibits human prostate cell growth via induction of mitochondrion-dependent cell apoptosis., Chin. J. Integr. Med. 18, 824–830 (2012). https://doi.org/10.1007/s11655-012-1264-y
Zhen-feng Hong, Jiu-mao Lin, Xiao-yong Zhong, et al. Qianliening capsule (前列宁胶囊) inhibits human prostate cell growth via induction of mitochondrion-dependent cell apoptosis[J]. Chinese Journal of Integrative Medicine, 2012,18(11):824-830.
Hong, Zf., Lin, Jm., Zhong, Xy. et al. Qianliening capsule (前列宁胶囊) inhibits human prostate cell growth via induction of mitochondrion-dependent cell apoptosis., Chin. J. Integr. Med. 18, 824–830 (2012). https://doi.org/10.1007/s11655-012-1264-yDOI:
Zhen-feng Hong, Jiu-mao Lin, Xiao-yong Zhong, et al. Qianliening capsule (前列宁胶囊) inhibits human prostate cell growth via induction of mitochondrion-dependent cell apoptosis[J]. Chinese Journal of Integrative Medicine, 2012,18(11):824-830. DOI: 10.1007/s11655-012-1264-y.
Qianliening capsule (前列宁胶囊) inhibits human prostate cell growth via induction of mitochondrion-dependent cell apoptosis
摘要
To investigate the molecular mechanisms by which Qianliening Capsule (前列宁胶囊
QC) treats benign prostatic hyperplasia (BPH). 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. 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. Promoting mitochondrion-dependent apoptosis of prostate stromal cells might be one of the mechanisms by which QC treats BPH.
Abstract
To investigate the molecular mechanisms by which Qianliening Capsule (前列宁胶囊
QC) treats benign prostatic hyperplasia (BPH). 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. 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. Promoting mitochondrion-dependent apoptosis of prostate stromal cells might be one of the mechanisms by which QC treats BPH.
Paolone DR. Benign prostatic hyperplasia. Clin Geriatr Med 2010;26:223–239.
Roehrborn CG. Male lower urinary tract symptoms (LUTS) and benign prostatic hyperplasia (BPH). Med Clin North Am 2011;95:87–100.
MacDonald R, Wilt TJ. Alfuzosin for treatment of lower urinary tract symptoms compatible with benign prostatic hyperplasia: a systematic review of efficacy and adverse effects. Urology 2005;66:780–788.
Roehrborn, Claus G. Efficacy and safety of once-daily alfuzosin in the treatment of lower urinary tract symptoms and clinical benign prostatic hyperplasia: a randomized, placebo-controlled trial. Urology 2001;58:953–959.
Djavan B, Marberger M. A meta-analysis on the efficacy and tolerability of α1-adrenoceptor antagonists in patients with lower urinary tract symptoms suggestive of Benign prostatic obstruction. European Urology 1999;36:1–13.
Gormley GJ, Stoner E, Bruskewitz RC, Imperato-McGinley J, Walsh PC, McConnell JD, et al. The effect of finasteride in men with benign prostatic hyperplasia. New Engl J Med 1992;327:1185–1191.
Roehrborn C, Boyle P, Nickel JC, Hoefner K, Andriole G. ARIA3001 ARIA3002 and ARIA3003 Study Investigators. Efficacy and safety of a dual inhibitor of 5-alpha-reductase types 1 and 2 (dutasteride) in men with benign prostatic hyperplasia. Urology 2002;60:434–441.
Boyle P, Robertson C, Lowe F, Roehrborn C. Meta-analysis of clinical trials of Permixon in the treatment of symptomatic benign prostatic hyperplasia. Urology 2000;55:533–539.
Wilt T, Ishani A, MacDonald R, Stark G, Mulrow C, Lau J. Beta-sitosterols for benign prostatic hyperplasia. Cochrane Database System Rev 2000;2:CD001043.
Wilt T, Ishani A, Mac Donald R, Rutks I, Stark G. Pygeum africanum for benign prostatic hyperplasia. Cochrane Database System Rev 2002;1:CD001044.
Zhou JH, Lin JM, Xu W, Zhong XY, Xie JD, Hong ZF. Effects of Qianliening capsule on the expression of IL-10 and TNF-α in benign prostatic hyperplasia. Chin Archiv Tradit Chin Med (Chin) 2010;28:2657–2569.
Zhou JH, Hong ZF, Lin JM, Zhao JY, Zhou HT. Effect of Qianliening Granule on experimental hyperplasia of prostate. J Fujian Univ Tradit Chin Med (Chin) 2008;18:45–47.
Zhou HT, Lin JM, Zhao JY, Zhou JH, Hong Zhenfeng. Inhibition effects of Qianliening Granule on IL-1β and its mRNA expression in model rats. J Fujian Univ Tradit Chin Med (Chin) 2010;20(3):21–24.
Barrack ER, Berry SJ. DNA synthesis in the canine Prostate:Effects of androgen and estrogen treatment. Prostate 1987;10:45.
Angelucci C, Iacopino F, Lama G, Zelano G, Gianesini G, Sica G, et al. Reverse transcriptase-PCR analysis of apoptosis-regulating gene expression in human benign prostatic hyperplasia. Anticancer Res 2005;25:3937–3941.
Pollan MC, Benghuzzi HA, Tucci M. Growth factor expression in early stages of benign prostatic hyperplasia upon exposure to sustained delivery of androgens. Biomed Sci Instrum 2003;39:329–34.
Cory S, Adams JM. The Bcl-2 family: regulators of the cellular life-of-death switch. Nature Rev Cancer 2002;2:647–656.
Adams JM, Cory S. The Bcl-2 apoptotic switch in cancer development and therapy. Oncogene 2007;26:1324–1337.
Gross A, McDonnell JM, Korsmeyer SJ. Bcl-2 family members and the mitochondria in apoptosis. Genes Dev 1999;13:1899–1911.
Jürgensmeier JM, Xie Z, Deveraux Q, Ellerby L, Bredesen D, Reed JC. Bax directly induces release of cytochrome c from isolated mitochondria. Proc Natl Acad Sci USA 1998;95:4997–5002.
Kluck RM, Bossy-Wetzel E, Green DR, Newmeyer DD. The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis. Science 1997;275:1132–1136.
Youle RJ, Strasser A. The BCL-2 protein family: opposing activities that mediate cell death. Nat Rev Mol Cell Biol 2008;9:47–59.
Yip KW, Reed JC. Bcl-2 family proteins and cancer. Oncogene 2008;27:6398–6406.