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Adult neural stem cell dysfunction in the subventricular zone of the lateral ventricle leads to diabetic olfactory defects 被引量:2
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作者 Yu-hong Jing Chu-chu Qi +3 位作者 Li Yuan Xiang-wen Liu Li-ping Gao Jie Yin 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第7期1111-1118,共8页
Sensitive smell discrimination is based on structural plasticity of the olfactory bulb,which depends on migration and integration of newborn neurons from the subventricular zone.In this study,we examined the relations... Sensitive smell discrimination is based on structural plasticity of the olfactory bulb,which depends on migration and integration of newborn neurons from the subventricular zone.In this study,we examined the relationship between neural stem cell status in the subventricular zone and olfactory function in rats with diabetes mellitus.Streptozotocin was injected through the femoral vein to induce type 1 diabetes mellitus in Sprague-Dawley rats.Two months after injection,olfactory sensitivity was decreased in diabetic rats.Meanwhile,the number of Brd U-positive and Brd U+/DCX+double-labeled cells was lower in the subventricular zone of diabetic rats compared with agematched normal rats.Western blot results revealed downregulated expression of insulin receptorβ,phosphorylated glycogen synthase kinase 3β,and β-catenin in the subventricular zone of diabetic rats.Altogether,these results indicate that diabetes mellitus causes insulin deficiency,which negatively regulates glycogen synthase kinase 3β and enhances β-catenin degradation,with these changes inhibiting neural stem cell proliferation.Further,these signaling pathways affect proliferation and differentiation of neural stem cells in the subventricular zone.Dysfunction of subventricular zone neural stem cells causes a decline in olfactory bulb structural plasticity and impairs olfactory sensitivity in diabetic rats. 展开更多
关键词 nerve regeneration diabetic encephalopathy adult neural stem cells olfactory function subventricular zone proliferation glycogen synthase kinase 3 beta β-catenin differentiation rats INSULIN type i diabetes mellitus neural regeneration
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