Expression of P-selectin in the penile vascular epithelia of smoking rats.
- Author:
Hua YANG
1
;
Dong-Wen WANG
;
Wei-Bing SHUANG
;
Jing-Qi WANG
;
Li ZHANG
;
Bin ZHAO
;
Jian ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Epithelium; metabolism; Male; P-Selectin; biosynthesis; Penile Erection; Penis; blood supply; metabolism; ultrastructure; Rats; Rats, Wistar; Smoking; adverse effects
- From: National Journal of Andrology 2008;14(12):1094-1098
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the expression of P-selectin in the penile vascular epithelial cells and the morphological changes in the ultrastructure of the penile cavernous tissues of smoking rats, and to explore the pathogenesis of smoking-induced erectile dysfunction.
METHODSFifty healthy Wistar rats were randomly divided into a normal control, a long-term heavy smoking group, a long-term light smoking, a short-term heavy smoking and a smoking cessation group. Their erectile function was tested by subcutaneous injection of apomorphine (APO), the P-selectin expression in the penile vascular epithelial cells detected by ELISA and the morphological changes in the ultrastructure of the penile cavernous tissues observed under the transmission electron microscope (TEM).
RESULTSThe levels of P-selectin were 10.78 +/- 1.71 ng/L, 62.62 +/- 5.95 ng/L, 40.06 +/- 3.97 ng/L, 41.37 +/- 4.06 ng/L and 22.80 +/- 3.15 ng/L respectively in the normal control, long-term heavy smoking, long-term light smoking, short-term heavy smoking and smoking cessation groups, with significant differences between the control group and the other four (P < 0.05). Electron microscopy showed abnormal arrangement of endothelia, penile cavernous sinuses and smooth muscle cells, disrupted continuity of endothelia, damaged ultrastructure of endothelial and smooth muscle cells in the penile cavernous tissue, and obvious proliferation and fibrosis of interstitial tissues in the smoking rats.
CONCLUSIONSmoking increases the P-selectin expression in the penile vascular epithelial cells and damages the ultrastructure of the penile cavernous tissue, which may be the main contributors to smoking-induced erectile dysfunction.