〔Abstract〕 Objective To analyze the expression of long non-coding RNA TALNEC2 in the middle cerebral artery occlusion(MCAO) model and oxygen-glucose deprivation(OGD) model, and to explore its regulatory mechanism in the process of acute cerebral infarction. Methods Anin vivomouse model of MCAO and anin vitrocell model of OGD were established to induce cerebral ischemic stroke condition.The expressions of TALNEC2,miR-19 a-3 p and c-jun-N-terminal kinase(JNK) were measured by qRT-PCR analysis.The neurological injuryin vivowas investigated by neurological score and TTC staining.Cell apoptosis and inflammatory injury were analyzed by Western blot, flow cytometry and ELISA,respectively.The interaction between miR-19 a-3 p and TALNEC2 or JNK was explored by luciferase activity assays. Results Up regulation of TALNEC2 was observed in MCAO and OGD models.Knockdown of TALNEC2 attenuated the cerebral infarct, neurological injury, apoptosis and inflammatory injury in MCAO mice.Luciferase activity analysis showed that miR-19 a-3 p combined with TALNEC2.Overexpression of miR-19 a-3 p inhibited the apoptosis and inflammatory response in OGD-treated brain microvascular endothelial cell(BMEC),which was attenuated by TALNEC2.JNK was a target of miR-19 a-3 p and its restoration reversed the miR-19 a-3 p-mediated suppression of apoptosis and inflammation.Moreover, TALNEC2 promoted JNK expression by competitively sponging miR-19 a-3 p. Conclusion The knockdown of TALNEC2 attenuates MCAO-or OGD-induced acute cerebral ischemia injury by regulating miR-19 a-3 p/JNK,which provides a new potential strategy for the treatment of acute cerebral infarction.