Hyperhomocysteinemia induces injury in olfactory bulb neurons by downregulating Hes1 and Hes5 expression

作     者：Jing-wen Zhang Bo Pang Qi Zhao Yue Chang Yi-li Wang Yi-deng Jiang Li Jing 

作者机构：School of Basic Medical ScienceNingxia Key Laboratory of Cerebrocranial Diseases-Incubation Base of National Key LaboratoryNingxiaMedical UniversityYinchuanNingxia Hui Autonomous RegionChina Institute of ImmunopathologyMedical SchoolKey Laboratory of Biomedical Information Engineering of Ministry of EducationXi'an JiaotongUniversityXi'anShaanxi ProvinceChina 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2018年第13卷第2期

页      面：272-279页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100204[医学-神经病学] 10[医学] 

基　　金：supported by the National Natural Science Foundation of China,No.81560084,81560208 a grant from the Project of Superior Discipline Groups in Ningxia Medical University of China,No.XY201414 

主　　题：nerve regeneration olfactory bulb apoptosis neurons Nissl body homocysteine hairy enhancer of split 1 hairy enhancer of split 5 neural regeneration 

摘      要：Hyperhomocysteinemia has been shown to be associated with neurodegenerative diseases; however, lesions or histological changes and mechanisms underlying homocysteine-induced injury in olfactory bulb neurons remain unclear. In this study, hyperhomocysteinemia was induced in apolipoprotein E-deficient mice with 1.7% methionine. Pathological changes in the olfactory bulb were observed through hematoxylin-eosin and Pischingert staining. Cell apoptosis in the olfactory bulb was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling （TUNEL） staining. Transmission electron microscopy revealed an abnormal ultrastructure of neurons. Furthermore, immunoreactivity and expression of the hairy enhancer of the split 1 （Hesl） and Hess were measured using immunohistochemistry, immunofluorescence, and western blot assay. Our results revealed no significant structural abnormality in the ol- factory bulb of hyperhomocysteinemic mice. However, the number of TUNEL-positive cells increased in the olfactory bulb, lipofuscin and vacuolization were visible in mitochondria, and the expression of Hes1 and Hes5 decreased. These findings confirm that hyperhomocyste- inemia induces injury in olfactory bulb neurons by downregulating Hes1 and Hes5 expression.