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目的观察不同吸烟量大鼠阴茎海绵体血管细胞间黏附分子-1(ICAM-1)的表达,探讨ICAM- 1在吸烟导致阴茎勃起功能障碍的发病机制中的作用及意义。方法健康雄性Wistar大鼠50只,分为正常对照组,长期大量吸烟组,长期小量吸烟组、短期大量吸烟组和戒烟组。造模完成后,皮下注射阿扑吗啡后纪录其勃起次数,采用双抗体夹心酶联免疫吸附法(ELISA)测定大鼠阴茎海绵体血管ICAM-1的含量水平。结果各实验组大鼠的阴茎勃起次数与对照组比较均明显减少(P<0-05)。正常对照组ICAM-1表达极少,长期大量组表达最高,长期小量组与短期大量组也有较高的表达,戒烟组表达明显降低,以上4组与对照组比较均有统计学差异(P<0.05)。ICAM-1表达与吸烟指数呈正相关(r=0.744)。结论香烟烟雾可使大鼠阴茎海绵体血管内皮细胞的ICAM-1表达增加,提示动脉粥样硬化可能是吸烟致阴茎勃起功能障碍的发病机制之一。
Objective To observe the expression of intercellular adhesion molecule-1 (ICAM-1) in corpus cavernosum of rats with different smoking levels and to explore the role and significance of ICAM-1 in the pathogenesis of smoking-induced erectile dysfunction. Methods Fifty healthy male Wistar rats were divided into normal control group, long-term heavy smoking group, long-term small smoking group, short-term heavy smoking group and smoking cessation group. After the model was established, the number of erection was recorded after subcutaneous injection of apomorphine, and the level of ICAM-1 in the corpus cavernosum was detected by double antibody sandwich enzyme-linked immunosorbent assay (ELISA). Results The number of penile erections in each experimental group was significantly decreased compared with the control group (P <0-05). The expression of ICAM-1 in normal control group was very low, the expression in long-term large group was the highest, the expression in long-term small group was also higher than that in short-term large group, and the expression in smoking cessation group was significantly lower than that in control group <0.05). ICAM-1 expression was positively correlated with smoking index (r = 0.744). Conclusion Cigarette smoke can increase ICAM-1 expression in rat corpus cavernosum vascular endothelial cells, suggesting that atherosclerosis may be one of the pathogenesis of smoking-induced erectile dysfunction.