{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zheng J"],"funding":["National Natural Science Foundation of China"],"pagination":["2792-2799"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6916328"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["235(3)"],"pubmed_abstract":["C-Jun N-terminal kinase (JNK) is a pivotal MAPK (mitogen-activated protein kinase), which activated by ischemia brain injury and plays a fairly crucial function in cerebral ischemic injury. Emerging studies demonstrated that JNK-IN-8 (a JNK inhibitor with high specificity) regulates traumatic brain injury through controlling neuronal apoptosis and inflammation. However, the function of JNK-IN-8 in ischemic stroke and the mechanisms underlying of JNK-IN-8 about neuroprotection are not well understood. In this work, male rats were treated with JNK-IN-8 after transient middle cerebral artery occlusion, and then the modified improved neurological function score (mNSS), the foot-fault test (FFT), interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) levels were assessed. We found th"],"journal":["Journal of cellular physiology"],"pubmed_title":["JNK-IN-8, a c-Jun N-terminal kinase inhibitor, improves functional recovery through suppressing neuroinflammation in ischemic stroke."],"pmcid":["PMC6916328"],"funding_grant_id":["81774109","81603685","81704180","81973620"],"pubmed_authors":["Zheng J","Han K","Geng W","Jia D","Dai Q","Fu H","Lv Y","Hong W","Mo Y","Tang H"],"additional_accession":[]},"is_claimable":false,"name":"JNK-IN-8, a c-Jun N-terminal kinase inhibitor, improves functional recovery through suppressing neuroinflammation in ischemic stroke.","description":"C-Jun N-terminal kinase (JNK) is a pivotal MAPK (mitogen-activated protein kinase), which activated by ischemia brain injury and plays a fairly crucial function in cerebral ischemic injury. Emerging studies demonstrated that JNK-IN-8 (a JNK inhibitor with high specificity) regulates traumatic brain injury through controlling neuronal apoptosis and inflammation. However, the function of JNK-IN-8 in ischemic stroke and the mechanisms underlying of JNK-IN-8 about neuroprotection are not well understood. In this work, male rats were treated with JNK-IN-8 after transient middle cerebral artery occlusion, and then the modified improved neurological function score (mNSS), the foot-fault test (FFT), interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) levels were assessed. We found th","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Mar","modification":"2025-04-04T11:39:33.618Z","creation":"2020-05-21T23:36:16Z"},"accession":"S-EPMC6916328","cross_references":{"pubmed":["31541462"],"doi":["10.1002/jcp.29183"]}}