Qianliening capsule treats benign prostatic hyperplasia via induction of prostatic cell apoptosis

被引:21
作者
Zheng, Haiyin [1 ]
Xu, Wei [2 ]
Lin, Jiumao [3 ]
Peng, Jun [3 ]
Hong, Zhenfeng [1 ]
机构
[1] Fujian Univ Tradit Chinese Med, Dept Integrat Med, Fuzhou 350122, Fujian, Peoples R China
[2] Fujian Univ Tradit Chinese Med, Dept Pharmacol, Fuzhou 350122, Fujian, Peoples R China
[3] Fujian Univ Tradit Chinese Med, Acad Integrat Med, Fuzhou 350122, Fujian, Peoples R China
关键词
Qianliening capsule; benign prostatic hyperplasia; Bcl-2; bax; caspase; 3; URINARY-TRACT SYMPTOMS; CHANNEL-FORMING ACTIVITY; CYTOCHROME-C; BCL-2; MITOCHONDRIA; BAX; RELEASE; EFFICACY; ALFUZOSIN; CYTOSOL;
D O I
10.3892/mmr.2013.1265
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The aim of this study was to evaluate the therapeutic efficacy of Qianliening capsule (QC) against benign prostatic hyperplasia (BPH) in vivo in a BPH rat model, as well as to investigate the effects of QC on prostatic cell apoptosis and the possible molecular mechanisms mediating its anti-BPH activity. Fifty male Sprague-Dawley (SD) rats were randomly classified into five groups. The rats of the four groups were castrated and subcutaneously injected with testosterone propionate to generate BPH. One week after model establishment, BPH rats were orally administrated with various doses of QC daily for 28 days. The prostatic tissues from BPH rats were collected to evaluate prostatic index (PI). The histological changes of prostate were observed by hematoxylin and eosin staining. TUNEL analysis was performed to examine cell apoptosis. The mRNA expression of Bcl-2 and Bax in prostatic tissues was determined by reverse transcription-polymerase chain reaction (RT-PCR). The protein expression of Bcl-2, Bax and cleaved caspase 3 were examined by immunohistochemistry. Administration with QC significantly decreased PI in a dose-dependent manner (P<0.05 or P<0.01) and improved prostatic hyperplasia in BPH rats. Additionally, QC treatment induced prostatic cell apoptosis in a dose-dependent manner. Moreover, QC promoted the cleavage of caspase 3, an indicator of apoptosis, in a dose-dependent manner. Furthermore, following QC treatment, the expression ratio of pro-apoptotic Bax to anti-apoptotic Bcl-2 in prostatic tissues was increased in a dose,dependent manner. As a result, QC was effective in the treatment of BPH in rats. Promoting apoptosis of prostatic cells may therefore be one of the mechanisms by which QC treats BPH.
引用
收藏
页码:848 / 854
页数:7
相关论文
共 34 条
[1]   The Bcl-2 apoptotic switch in cancer development and therapy [J].
Adams, J. M. ;
Cory, S. .
ONCOGENE, 2007, 26 (09) :1324-1337
[2]   Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria [J].
Antonsson, B ;
Montessuit, S ;
Lauper, S ;
Eskes, R ;
Martinou, JC .
BIOCHEMICAL JOURNAL, 2000, 345 :271-278
[3]   Inhibition of Bax channel-forming activity by Bcl-2 [J].
Antonsson, B ;
Conti, F ;
Ciavatta, A ;
Montessuit, S ;
Lewis, S ;
Martinou, I ;
Bernasconi, L ;
Bernard, A ;
Mermod, JJ ;
Mazzei, G ;
Maundrell, K ;
Gambale, F ;
Sadoul, R ;
Martinou, JC .
SCIENCE, 1997, 277 (5324) :370-372
[4]   THE DEVELOPMENT OF HUMAN BENIGN PROSTATIC HYPERPLASIA WITH AGE [J].
BERRY, SJ ;
COFFEY, DS ;
WALSH, PC ;
EWING, LL .
JOURNAL OF UROLOGY, 1984, 132 (03) :474-479
[5]  
Black L, 2006, AM J MANAG CARE, V12, pS99
[6]   Cell kinetic in epithelium and stroma of benign prostatic hyperplasia [J].
Claus, S ;
Berges, R ;
Senge, T ;
Schulze, H .
JOURNAL OF UROLOGY, 1997, 158 (01) :217-221
[7]   Lower urinary tract symptoms/benign prostatic hyperplasia: Fast control of the patient's quality of life [J].
Djavan, B .
UROLOGY, 2003, 62 (3A) :6-14
[8]   A meta-analysis on the efficacy and tolerability of α1-adrenoceptor antagonists in patients with lower urinary tract symptoms suggestive of benign prostatic obstruction [J].
Djavan, B ;
Marberger, M .
EUROPEAN UROLOGY, 1999, 36 (01) :1-12
[9]   THE EFFECT OF FINASTERIDE IN MEN WITH BENIGN PROSTATIC HYPERPLASIA [J].
GORMLEY, GJ ;
STONER, E ;
BRUSKEWITZ, RC ;
IMPERATOMCGINLEY, J ;
WALSH, PC ;
MCCONNELL, JD ;
ANDRIOLE, GL ;
GELLER, J ;
BRACKEN, BR ;
TENOVER, JS ;
VAUGHAN, ED ;
PAPPAS, F ;
TAYLOR, A ;
BINKOWITZ, B ;
NG, J .
NEW ENGLAND JOURNAL OF MEDICINE, 1992, 327 (17) :1185-1191
[10]   BCL-2 family members and the mitochondria in apoptosis [J].
Gross, A ;
McDonnell, JM ;
Korsmeyer, SJ .
GENES & DEVELOPMENT, 1999, 13 (15) :1899-1911