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Autophagy has been implicated in the regulation of neuroinflammation and neurodegenerative disorders. Licochalcone B (LCB), a chalcone from <i>Glycyrrhiza inflata</i>, has been reported to have anti-cancer, anti-oxidation and anti-β–amyloid fibrillation effects; however, its effect in autophagy remain un-investigated. In the current study, the potential neuro-protective role of LCB in terms of its anti-oxidative, anti-apoptotic, and autophagic properties upon oxidative stress-induced damage in neuronal cells was investigated. With the production of reactive oxygen species (ROS) as a hallmark of neuroinflammation and neurodegeneration, hydrogen peroxide (H₂O₂) was adopted to stimulate ROS-induced cell apoptosis in PC-12 cells. Our findings revealed that LCB reduced cell cytotoxicity and apoptosis of PC-12 cells upon H₂O₂-stimulation. Furthermore, LCB increased the level of the apoptosis-associated proteins caspase-3 and cleaved caspase-3 in H₂O₂-induced cells. LCB effectively attenuated the level of oxidative stress markers such as MDA, SOD, and ROS in H₂O₂-induced cells. Most importantly, LCB was confirmed to possess its anti-apoptotic effects in H₂O₂-induced cells through the induction of ATG7-dependent autophagy and the SIRT1/AMPK signaling pathway. As a novel autophagic inducer, LCB increased the level of autophagy-related proteins LC3–II and decreased p62 in both neuronal cells and <i>Caenorhabditis elegans</i> (<i>C. elegans</i>) models. These results suggested that LCB has potential neuroprotective effects on oxidative damage models via multiple protective pharmacological mechanisms.