Folic acid deficiency increases brain cell injury via autophagy enhancement after focal cerebral ischemia

• Published in: The Journal of nutritional biochemistry Vol. 38; pp. 41 - 49
• Main Authors: Zhao, Yaqian, Huang, Guowei, Chen, Shuang, Gou, Yun, Dong, Zhiping, Zhang, Xumei
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2016
• Subjects: Adenine - analogs & derivatives; Adenine - therapeutic use; Animals; Autophagosomes - drug effects; Autophagosomes - metabolism; Autophagosomes - pathology; Autophagosomes - ultrastructure; Autophagy; Autophagy - drug effects; Beclin-1 - metabolism; Biomarkers - metabolism; brain; brain damage; Brain Ischemia - complications; Brain Ischemia - metabolism; Brain Ischemia - pathology; Cell Body - drug effects; Cell Body - metabolism; Cell Body - pathology; Cell Body - ultrastructure; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Cerebral Cortex - pathology; Cerebral Cortex - ultrastructure; Cerebral ischemia–reperfusion; Cortex; DNA; DNA damage; DNA Damage - drug effects; folic acid; Folic acid deficiency; Folic Acid Deficiency - complications; Folic Acid Deficiency - metabolism; Folic Acid Deficiency - pathology; ischemia; Male; Microscopy, Electron, Transmission; Microtubule-Associated Proteins - metabolism; Nerve Tissue Proteins - metabolism; neurons; Neurons - drug effects; Neurons - metabolism; Neurons - pathology; Neurons - ultrastructure; Oxidative stress; Oxidative Stress - drug effects; Random Allocation; rats; Rats, Sprague-Dawley; Reperfusion Injury - prevention & control; risk; Specific Pathogen-Free Organisms; stroke; Up-Regulation - drug effects; Oxidative stress; Folic acid deficiency; Autophagy; Cerebral ischemia–reperfusion; Cortex

Folic acid (FA) deficiency is not only associated with an increased risk of ischemic stroke, but also with increased oxidative DNA damage and brain injury after cerebral ischemia–reperfusion. However, the cellular and molecular mechanisms underlying FA deficiency-associated neuropathogenesis are not...