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Issue Cover (August 2020)
Publication year - 2020
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.14755
Subject(s) - autophagy , apoptosis , flux (metallurgy) , traumatic brain injury , valproic acid , programmed cell death , cover (algebra) , brain function , medicine , neuroscience , cancer research , chemistry , psychology , psychiatry , epilepsy , biochemistry , mechanical engineering , organic chemistry , engineering
Front cover: Appropriate levels of autophagy can promote the removal of abnormal proteins or damaged organelles, while hyperactivated autophagy can induce autophagic apoptosis. However, it was reported that autophagic flux may be blocked after traumatic brain injury (TBI), which may further cause brain cells apoptosis. Here, we found that daily intraperitoneal injection of valproic acid (VPA) after TBI for three days may contribute to lysosomal function recovery to reverse TBI‐induced autophagic flux blockage, which is accompanied by reduced inflammatory response and decreased brain cell apoptosis. Furthermore, 3‐methyladenine (3‐MA) administration for inhibiting autophagy in VPA‐treated injured mice abolished VPA‐induced neuroprotective and anti‐inflammatory effects, which results in significantly reduced neurite expression when immunofluorescent staining with anti‐NeuN and anti‐MAP2 antibodies in the somatosensory cortical region. Our findings support that VPA treatment after TBI contributes to functional recovery via enhancing autophagic flux. Image content: Immunofluorescence staining was performed at 3 days post injury on VPA‐treated injured mice with 3‐MA pretreatment. DAPI (blue cannel), MAP2 (green cannel) and NeuN (red cannel) were utilized to mark the brain cells nuclear, neurites and neurons in mouse brain tissue, respectively. The tissue was mounted after incubation with the corresponding secondary antibody and captured by a Nikon ECLIPSE 80i microscope. Pretreatment with 3‐MA in VPA‐treated mice suffering from TBI resulted in significant down‐regulation of neuronal neurite expression in the somatosensory cortex around the lesion, indicating that 3‐MA pretreatment partially abolished VPA‐induced neuroprotective effect after TBI.Read the full article ‘Valproic acid affects neuronal fate and microglial function via enhancing autophagic flux in mice after traumatic brain injury’ by Z. Zheng, Y. Wu, Z. Li, L. Ye, Q. Lu, Y. Zhou, Y. Yuan, T. Jiang, L. Xie, Y. Liu, D. Chen, J. Ye, W. Nimlamool, H. Zhang, J. Xiao, ( J. Neurochem . 2020, vol. 154 (3), pp. 284–300) on doi: 10.1111/jnc.14892