Share this post on:

Le of TRPC1 channels. J Neurosci. 2012;32:9835?7. 61. Yao H, Bethel-Brown C, Buch
Le of TRPC1 channels. J Neurosci. 2012;32:9835?7. 61. Yao H, Bethel-Brown C, Buch S. Cocaine exposure results in formation of dendritic varicosity in rat primary hippocampal neurons. Am J Infect Dis. 2009;5:26?0. 62. Yao H, Duan M, Buch S. Cocaine-mediated induction of platelet-derived growth factor: implication for increased vascular buy Nectrolide permeability. Blood. 2011; 117:2538?7. 63. Dhillon NK, Williams R, Peng F, Tsai YJ, Dhillon S, Nicolay B, et al. Cocainemediated enhancement of virus replication in macrophages: implications for human immunodeficiency virus-associated dementia. J Neurovirol. 2007; 13:483?5. 64. Guo ML, Liao K, Periyasamy P, Yang L, Cai Y, Callen SE, et al. Cocaine mediated microglial activation involves the ER stress-autophagy axis. Autophagy. 2015;11(7):995?009. 65. Yang L, Yao H, Chen X, Cai Y, Callen S, Buch S. Role of sigma receptor in cocaine-mediated induction of glial fibrillary acidic protein: implications for HAND. Mol Neurobiol. 2015. doi:10.1007/s12035-015-9094-5..Submit your next manuscript to BioMed Central and we will help you at every step:?We accept pre-submission inquiries ?Our selector tool helps you to find the most relevant journal ?We provide round the clock customer support ?Convenient online submission ?Thorough peer review ?Inclusion in PubMed and all major indexing services ?Maximum visibility for your research Submit your manuscript at www.biomedcentral.com/submit
Park and Sohrabji Journal of Neuroinflammation (2016) 13:300 DOI 10.1186/s12974-016-0765-RESEARCHOpen AccessThe histone deacetylase inhibitor, sodium butyrate, exhibits neuroprotective effects for ischemic stroke in middle-aged female ratsMin Jung Park and Farida Sohrabji*AbstractBackground: Sodium butyrate (NaB) is a histone deacetylase (HDAC) inhibitor exhibiting anti-inflammatory and neuroprotective effects in a rat ischemic model of stroke as well as a myocardial ischemia model. Although clinical evidence shows that older women are at higher risk for stroke occurrence and greater stroke severity, no studies have evaluated the effectiveness of NaB either in females or in older animals. Methods: To determine the effects of NaB on stroke in older females, acyclic middle-aged Sprague-Dawley female rats (9?1 months old, constant diestrus) were subject to middle cerebral artery occlusion (MCAo) by intracerebral injection of recombinant endothelin-1. Rats were treated with NaB (300 mg/kg, i.p.) at 6 and 30 h following ET-1 injection. Animals were sacrificed at the early (2 days) or late (5 days) acute phase after MCAo. Serum and tissue lysates were collected for biochemical analyses. Results: NaB treatment reduced infarct volume and ameliorated sensory motor impairment in middle-aged female rats, when measured at 2 and 5 days post MCAo. At the early acute phase (2 days post stroke), NaB treatment decreased brain lipid peroxides, and reduced serum levels of GFAP, a surrogate marker of blood-brain barrier (BBB) permeability. NaB also reduced expression of the inflammatory cytokine IL-1beta in circulation and IL-18 in the ischemic hemisphere. At the late acute phase (5 days post PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28212752 stroke), NaB treatment further suppressed MCAo-induced increase of IL-1beta, IL-17A, and IL-18 in brain lysates (cortex and striatum) from the ischemic hemisphere, and decreased ischemia-induced upregulation of IL-1beta and IL-18 in circulation, indicating a potent anti-inflammatory effect of the HDAC inhibitor. Moreover, NaB treatment also increased expression of IGF-1.

Share this post on: