Objective To investigate the efficacy and mechanism of c-Jun N-terminal kinase (JNK) in boosting survival of oxygen glucose deprivation (OGD) rat neurons. Methods The cortex neurons from fetal rats were primarily cultured to prepare a model of OGD neurons in vitro, and the characteristic endpoints were filtered to intervene with JNK inducer anisomycin (AN), respectively. The cells were randomly divided into control group, solvent control group (a same volume of solvent DMSO was added into the culture medium of the OGD neuron), AN group (OGD neurons were treated with JNK inducer AN for 5 hours at the end of OGD). After that, Western blotting and immunofluorescence cytometry were respectively performed to detect the protein expressions in OGD neurons, including beclin 1, microtubule-associated protein 1 light chain 3 (LC3), B cell lymphoma 2 (Bcl2), caspase-3, P62, ubiquitin, cathepsin B and lysosomal associated membrane protein 1 (LAMP1). The cell activity was evaluated by CCK-8 assay, and the axon length was measured by IPP software. Results Activation of JNK significantly promoted the expressions of beclin 1, LC3, and Bcl2, and markedly reduced the content of beclin 1-Bcl2 complex and attenuated the expressions of P62 and ubiquitin. Meanwhile, the expressions of cathepsin B and LAMP1 were not obviously altered. In this way, the survival rate of OGD neurons was improved. Conclusion Activation of JNK exerts a neuroprotective effect by facilitating dissociation of beclin 1-Bcl2 and inducing a switch from apoptosis to autophagy in OGD neurons.