FDCA Attenuates Neuroinflammation and Brain Injury after Cerebral Ischemic Stroke

experiments further demonstrated that FDCA disrupted the phosphorylations of myosin phosphatase target subunit 1 (MYPT1), mitogen-activated protein kinase (MAPK) cascade, including p38 and c-Jun N-terminal kinase (JNK), and pyruvate dehydrogenase (PDH) and limited excessive lactic acid metabolites, resulting in inhibition of BBB disruption and neuroinflammation. In addition, FDCA potently mitigated inflammatory response in human monocytes isolated from ischemic stroke patients, which provides the possibilities of a clinical translation perspective. Overall, these findings provided a therapeutic potential for FDCA as a candidate agent for ischemic stroke and other neurological diseases associated with BBB disruption and neuroinflammation.