摘要
目的:以大鼠脾脏为模型,探讨平阳霉素治疗海绵状血管瘤的机制。方法:观察平阳霉素注射于大鼠脾脏后不同时段的病理变化,采用末端转移酶介导的缺口末端标记法结合透射电镜检测凋亡,图像分析技术选择性地比较不同作用时段的凋亡率,免疫组化结合图像分析仪定量分析凋亡相关蛋白Caspase-3的变化。结果:注射生理盐水不引起大鼠脾脏结构破坏。注射平阳霉素后第2天、第5天脾脏仅有轻微肿胀;第8天、第14天呈萎缩改变,脾窦内皮细胞受损伤;注射平阳霉素后不同时间电镜检查均可见到凋亡细胞;TUNEL标记结果显示凋亡广泛发生于脾窦内皮细胞及其他脾细胞;注射后一定时间内,凋亡率随作用时间延长而增加;Caspase-3蛋白表达逐渐增强,与细胞凋亡的增加一致。结论:平阳霉素主要通过诱导脾窦内皮细胞凋亡为主,并导致一定程度的坏死,少量的成纤维细胞增生等。其发生机制是通过Caspase-3活化途径来诱导细胞凋亡。
Objective： To investigate the mechanism of Pingyangmycin in treatment of cavernous hemangioma using rat spleen as a model. Methods： The pathological changes of rat spleen were observed on different time points after Pingyangmycin was injected into the rat spleen. Cell apoptosis was verified with TUNEL staining and transmission electron microscope; the expression of apoptosis-related protein caspase-3 was detected with immunohistochemical method and image analysis system. Resuits： Injecting saline into rat spleen caused no damage to the spleen. Slight swelling was observed on d 2 and d 5 after Pingyangmycin was injected and the spleen became shrunk （with damaged-splenic sinus） on d 8 and d 14. Apoptotic cells were found on different days after Pingyangmycin injection under transmission electron microscope. TUNEL staining indicated that apoptotic cells existed extensively in endothelial cells of splenic sinus and others splenic cells. Apoptosis rate increased with time during a certain period of time after Pingyangmycin injection and caspase-3 expression increased gradually with the increase of apoptosis rate. Conclusion： Pingyangmycin causes necrosis of spleen mainly through inducing apoptosis; it can also cause necrosis and slight fibroblast cell hyperplasia. The apoptosis induction process is dependent on caspase-3 activation process.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2006年第2期178-181,共4页
Academic Journal of Second Military Medical University
