Keywords: Brain trauma, Hydrogen sulfide, Neurotrophic element, Inflammation, Motor recovery, Infarct region, Infarct volume, Nitrosative pressure, Astrogliosis, Neuroprotection* Correspondence: email@example.com Equal contributors 1 Department of Biological and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D'Alcontres, 31-98166 Messina, Italy three Manchester order PF-4708671 Biomedical Analysis Centre,.O test the specificity of antibodies for cannabinoid receptors. Lopez-Rodriguez AB, Siopi E, Finn DP, Marchand-Leroux C, Garcia-Segura LM, Jafarian-Tehrani M, Viveros MP: CB1 and CB2 cannabinoid receptor antagonists protect against 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, such as dynamic interplay among 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 useful 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 decreasing the secondary inflammation and tissue injury. Techniques: Here we evaluated the neuroprotective possible of ATB-346, a hydrogen sulfide-releasing derivative of naproxen, working with the controlled cortical effect (CCI) injury model in mice, one of one of the most popular models of TBI. Additionally, the aim from the present study was to cautiously investigate molecular pathways and subtypes of glial cells involved within the protective effect of ATB-346 on inflammatory reaction connected with an experimental model of TBI. In these research, TBI was induced in mice by CCI and mice have been orally administered ATB-346, naproxen (each at 30 mol/kg) or vehicle (dimethylsulfoxide:1 carboxymethylcellulose [5:95] suspension) one and six hours soon after brain trauma and once every day for 10 days. Outcomes: Results revealed that ATB-346 attenuated TBI-induced brain edema, suppressed TBI-induced neural cell death and improved neurological function. ATB-346 also drastically lowered the severity of inflammation and restored neurotrophic aspects that characterized the secondary events of TBI. Conclusions: These information demonstrate that ATB-346 is often efficacious in a TBI animal model by lowering the secondary inflammation and tissue injury. Consequently, ATB-346 could represent an exciting approach for the management of secondary harm following CNS diseases, counteracting behavioral modifications and inflammatory procedure. Keywords and phrases: Brain trauma, Hydrogen sulfide, Neurotrophic factor, Inflammation, Motor recovery, Infarct location, Infarct volume, Nitrosative tension, Astrogliosis, Neuroprotection* Correspondence: firstname.lastname@example.org Equal contributors 1 Division of Biological and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D'Alcontres, 31-98166 Messina, Italy three Manchester Biomedical Analysis Centre,.