摘要
目的研究KKAy小鼠的脑微血管病变,明确糖尿病脑络病理变化的具体表现。方法 9~11周龄雄性KKAy小鼠和对照组的雄性C57BL/J小鼠,测量16、20、24、28周龄小鼠空腹血糖和体重。28周时处死动物,测定血清6-Keto-PGF1α和TXB2含量。光镜和电镜观察脑组织病理形态。结果 KKAy小鼠体重、血糖比同龄对照组C57BL/J小鼠高,血清TXB2含量增高,6-Keto-PGF1α降低。KKAy小鼠脑微血管内皮细胞核肿大,管腔狭小,腔内有红细胞、血小板淤滞。神经细胞胞核疏松肿胀,线粒体轻微肿胀,粗面内质网较瘦小,核糖小体减少。结论在高血糖和异常6-Keto-PGF1α和TXB2含量的毒性作用下,KKAy小鼠脑组织微血管内皮细胞结构和功能均有损伤,最终导致神经细胞结构破坏。
Objective To study the pathological changes of cerebral capillary in KKAy mice, and determine the specific manifestations of brain collateral disease of diabetes. Methods Male KKAy mice （9-11 weeks old） were included into the model group and male C57BL/J mice （9-11 weeks old） were included into the control group. The fasting plasma glucose and body weight were measured in mice of 16, 20, 24 and 28 weeks old respectively, and on the 28th week all mice were sacrificed. The serum content of 6-Keto-PGF1α and TXB2 were detected. The brain pathomorphological changes were observed with the light microscope and transmission electron microscope （TEM）. Results Compared with C57BL/J mice, in KKAy mice the levels of weight and plasma glucose were higher, serum content of TXB2 increased and serum content of 6-Keto-PGF1α deceased. The nuclei of brain capillary endothelial cells were loose and swollen, lumen became narrow with stasis of erythrocytes and platelets, nuclei and mitochondria of nerve cells were swollen, rough endoplasmic reticulum became extenuation, and ribosome reduced. Conclusion The structure and function of brain capillary endothelial cells are injured by higher plasma glucose and abnormal serum content of 6-Keto-PGF1α and TXB2, which will induce the destroy of neurocyte structure finally.
出处
《北京中医药大学学报》
CAS
CSCD
北大核心
2010年第5期327-329,345,I0001,共5页
Journal of Beijing University of Traditional Chinese Medicine
基金
国家自然科学基金资助项目(No.30572437
No.30672756)
