NDRG4 prevents cerebral ischemia/reperfusion injury by inhibiting neuronal apoptosis

التفاصيل البيبلوغرافية
العنوان: NDRG4 prevents cerebral ischemia/reperfusion injury by inhibiting neuronal apoptosis
المؤلفون: Lan Wen, Qinbin Zhang, Changqing Li, Keming Zhang, Linyan Tong, Jinfang Li, Lei Liu
المصدر: Genes and Diseases, Vol 6, Iss 4, Pp 448-454 (2019)
Genes & Diseases
بيانات النشر: Elsevier, 2019.
سنة النشر: 2019
مصطلحات موضوعية: 0301 basic medicine, lcsh:QH426-470, Ischemia, Apoptosis, Biochemistry, Article, 03 medical and health sciences, 0302 clinical medicine, medicine, NDRG4, Molecular Biology, Genetics (clinical), Neuronal apoptosis, lcsh:R5-920, business.industry, Cell Biology, medicine.disease, Reperfusion injury, lcsh:Genetics, BDNF, 030104 developmental biology, Cancer research, business, lcsh:Medicine (General), 030217 neurology & neurosurgery
الوصف: Cerebral ischemia is a major cause of mortality and long-term morbidity worldwide. NDRG4 has been shown to protect against cerebral ischemia, although the underlying mechanisms remain largely unclear. Here we found that NDRG4 expression was decreased in the brain tissues of ischemia/reperfusion (IR) rats, indicating increased apoptosis rates among cerebral cells. NDRG4 restoration via an adenovirus significantly attenuated cerebral infarct sizes and impairments in IR rats. Furthermore, adenovirus-mediated NDRG4 inhibited cell apoptosis in the brains of IR rats and regulated the expression of Bcl-2, Bax, caspase-3, and c-Fos. Moreover, we found that NDRG4 increased expression of BDNF, which is strongly related to cerebral ischemia and cellular apoptosis. Altogether, our findings demonstrate that NDRG4 protects cerebral IR injury by inhibiting cell apoptosis and regulates cerebral cell apoptosis by increasing BDNF expression. These results suggest that NDRG4 may be a therapeutic target for IR treatment. Keywords: Apoptosis, BDNF, Ischemia, NDRG4, Reperfusion injury
اللغة: English
تدمد: 2352-3042
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::816cc7dad1f13099864c69056efd3872
http://www.sciencedirect.com/science/article/pii/S2352304218301260
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....816cc7dad1f13099864c69056efd3872
قاعدة البيانات: OpenAIRE