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O test the specificity of antibodies for cannabinoid receptors. Hippocampus 2012, 22:643?44. 62. Atwood

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PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28461567 Journal of Neuroinflammation 2014, 11:196 http://www.jneuroinflammation.com/content/11/1/JOURNAL OF NEUROINFLAMMATIONRESEARCHOpen AccessHydrogen sulfide-releasing cyclooxygenase inhibitor ATB-346 enhances motor function and reduces cortical lesion volume following traumatic brain injury in miceMichela Campolo1, Emanuela Esposito1, Akbar Ahmad1, Rosanna Di Paola1, Irene Paterniti1, Marika Cordaro1, Giuseppe Bruschetta1, John L Wallace2 and Salvatore Cuzzocrea1,3*AbstractBackground: Traumatic brain injury (TBI) induces For 30 s and 72 for 30 s; and one particular cycle at 72 for 7 min. secondary injury mechanisms, which includes dynamic interplay among ischemic, inflammatory and cytotoxic processes. Keyword phrases: Brain trauma, Hydrogen sulfide, Neurotrophic element, Inflammation, Motor recovery, Infarct region, Infarct volume, L the earliest sign of impairment of retinal and optic nerve Nitrosative pressure, Astrogliosis, Neuroprotection* Correspondence: salvator@unime.it Equal contributors 1 Department of Biological and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D'Alcontres, 31-98166 Messina, Italy 3 Manchester Biomedical Study Centre,.O test the specificity of antibodies for cannabinoid receptors. Hippocampus 2012, 22:643?44. 62. Atwood BK, Mackie K: CB2: a cannabinoid receptor with an identity crisis. Br J Pharmacol 2010, 160:467?79. 63. Lopez-Rodriguez AB, Siopi E, Finn DP, Marchand-Leroux C, Garcia-Segura LM, Jafarian-Tehrani M, Viveros MP: CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cereb Cortex 2013. doi:10.1093/cercor/ bhtdoi:10.1186/s12974-014-0191-6 Cite this article as: Amenta et al.: Cannabinoid receptor type-2 stimulation, blockade, and deletion alter the vascular inflammatory responses to traumatic brain injury. Journal of Neuroinflammation 2014 11:191. Campolo et al. PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28461567 Journal of Neuroinflammation 2014, 11:196 http://www.jneuroinflammation.com/content/11/1/JOURNAL OF NEUROINFLAMMATIONRESEARCHOpen AccessHydrogen sulfide-releasing cyclooxygenase inhibitor ATB-346 enhances motor function and reduces cortical lesion volume following traumatic brain injury in miceMichela Campolo1, Emanuela Esposito1, Akbar Ahmad1, Rosanna Di Paola1, Irene Paterniti1, Marika Cordaro1, Giuseppe Bruschetta1, John L Wallace2 and Salvatore Cuzzocrea1,3*AbstractBackground: Traumatic brain injury (TBI) induces secondary injury mechanisms, which includes dynamic interplay involving ischemic, inflammatory and cytotoxic processes. We not too long ago reported that administration of ATB-346 (2-(6-methoxynapthalen- 2-yl)-propionic acid 4-thiocarbamoyl-phenyl ester), a hydrogen sulfide-releasing cyclooxygenase inhibitor, showed marked helpful effects in an animal PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27689333 model of spinal cord injury, significantly enhancing recovery of motor function and reducing the secondary inflammation and tissue injury. Strategies: Here we evaluated the neuroprotective potential of ATB-346, a hydrogen sulfide-releasing derivative of naproxen, making use of the controlled cortical influence (CCI) injury model in mice, among probably the most popular models of TBI. In addition, the aim from the present study was to very carefully investigate molecular pathways and subtypes of glial cells involved within the protective effect of ATB-346 on inflammatory reaction linked with an experimental model of TBI. In these studies, TBI was induced in mice by CCI and mice have been orally administered ATB-346, naproxen (each at 30 mol/kg) or car (dimethylsulfoxide:1 carboxymethylcellulose [5:95] suspension) one particular and six hours following brain trauma and once everyday for 10 days. Benefits: Results revealed that ATB-346 attenuated TBI-induced brain edema, suppressed TBI-induced neural cell death and enhanced neurological function. ATB-346 also substantially decreased the severity of inflammation and restored neurotrophic components that characterized the secondary events of TBI. Conclusions: These data demonstrate that ATB-346 may be efficacious within a TBI animal model by lowering the secondary inflammation and tissue injury.