<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zheng J</submitter><funding>National Natural Science Foundation of China</funding><pagination>2792-2799</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6916328</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>235(3)</volume><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</pubmed_abstract><journal>Journal of cellular physiology</journal><pubmed_title>JNK-IN-8, a c-Jun N-terminal kinase inhibitor, improves functional recovery through suppressing neuroinflammation in ischemic stroke.</pubmed_title><pmcid>PMC6916328</pmcid><funding_grant_id>81774109</funding_grant_id><funding_grant_id>81603685</funding_grant_id><funding_grant_id>81704180</funding_grant_id><funding_grant_id>81973620</funding_grant_id><pubmed_authors>Zheng J</pubmed_authors><pubmed_authors>Han K</pubmed_authors><pubmed_authors>Geng W</pubmed_authors><pubmed_authors>Jia D</pubmed_authors><pubmed_authors>Dai Q</pubmed_authors><pubmed_authors>Fu H</pubmed_authors><pubmed_authors>Lv Y</pubmed_authors><pubmed_authors>Hong W</pubmed_authors><pubmed_authors>Mo Y</pubmed_authors><pubmed_authors>Tang H</pubmed_authors></additional><is_claimable>false</is_claimable><name>JNK-IN-8, a c-Jun N-terminal kinase inhibitor, improves functional recovery through suppressing neuroinflammation in ischemic stroke.</name><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</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Mar</publication><modification>2025-04-04T11:39:33.618Z</modification><creation>2020-05-21T23:36:16Z</creation></dates><accession>S-EPMC6916328</accession><cross_references><pubmed>31541462</pubmed><doi>10.1002/jcp.29183</doi></cross_references></HashMap>