<jats:p><jats:italic>Objective</jats:italic>. This study is aimed at studying the effect of quercetin on the Alzheimer disease cell model induced by A<jats:italic>β</jats:italic><jats:sub>25-35</jats:sub> in PC12 cells and its mechanism of action. <jats:italic>Methods</jats:italic>. The AD cell model was established by A<jats:italic>β</jats:italic><jats:sub>25-35</jats:sub>. Quercetin was used at different concentrations (0, 10, 20, 40, and 80 <jats:italic>μ</jats:italic>mol/L). The morphology of cells was observed, and the effect on cell survival rate was detected by the MTT method. Cell proliferation was detected by the SRB method. The contents of LDH, SOD, MDA, GSH-Px, AChE, CAT, and T-AOC were detected by kits. The expression of sirtuin1/Nrf2/HO-1 was detected by RT-qPCR and Western blot. <jats:italic>Results</jats:italic>. PC12 cells in the control group grew quickly and adhered well to the wall, most of which had extended long axons and easily grew into clusters. In the model group, cells were significantly damaged and the number of cells was significantly reduced. It was found that PC12 cells were swollen, rounded, protruding, and retracting, with reduced adherent function and floating phenomenon. Quercetin could increase the survival rate and proliferation rate of PC12 cells; reduce the levels of LDH, AChE, MDA, and HO-1 protein; and increase the levels of SOD, GSH-Px, CAT, T-AOC, sirtuin1, and Nrf2 protein. <jats:italic>Conclusion</jats:italic>. Quercetin can increase the survival rate of PC12 injured by A<jats:italic>β</jats:italic><jats:sub>25-35</jats:sub>, promote cell proliferation, and antagonize the toxicity of A<jats:italic>β</jats:italic>; it also has certain neuroprotective effects. Therefore, quercetin is expected to become a drug for the treatment of AD.</jats:p>