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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 brain microvessels in KKAy mice and clarify the specific pathological changes of diabetic brain. Methods Male C57BL / J mice of 9 to 11 weeks old male KKAy mice and control group were used to measure fasting blood glucose and body weight of mice at 16, 20, 24 and 28 weeks. At 28 weeks, animals were sacrificed and serum 6-Keto-PGF1α and TXB2 levels were determined. Light microscopy and electron microscopy of brain tissue pathology. Results The body weight and blood glucose of KKAy mice were higher than that of C57BL / J mice of the same age. The content of TXB2 and the content of 6-Keto-PGF1α were decreased. KKAy mouse brain microvascular endothelial cell enlargement, narrow lumen, intracavitary red blood cells, platelet stasis. Nerve cell nucleus loose swelling, mild mitochondria swelling, rough endoplasmic reticulum is relatively small, ribosomes reduced. Conclusions Under the action of hyperglycemia and abnormal 6-Keto-PGF1α and TXB2 levels, the structure and function of microvascular endothelial cells in KKAy mice are damaged, eventually leading to the destruction of nerve cell structure.