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Neuroprotective effects of bornyl acetate against okadaic acid–Induced cytotoxicity in pc12 cells via beclin-1-dependent autophagy pathway

Background: β-amyloid (Aβ) deposition and tau protein abnormality are the major pathogenesis of Alzheimer's disease (AD). Autophagy is contributed to eliminating the misfolded proteins or organelles and alleviated cellular injury. Our pre-experimental findings showed that bornyl acetate (BA), the main component of the volatile oil of Amomum villosum, has a neuroprotective effect in okadaic acid (OA)–induced PC12 cells. However, the protective mechanism of autophagy that BA relieves OA-induced cellular injury is still unclear. Objectives: The purpose of our experiment was to elucidate the mechanism of treatment of AD. Materials and Methods: To explore how BA has therapeutic effects on AD, a model of OA-induced PC12 cells was established. The OA modelling induction and BA treatment in cells were evaluated by LDH and CCK-8 methods; ELISA assay was used to detect the tau hyperphosphorylation (p-tau), Aβ42 and β-secretase levels; The expression of p-Akt and p-mTOR were detected by western blot analysis; and immunohistochemical, immunofluorescence methods and western blot analysis were used to detect Beclin-1 expression. Autophagosomes in each group were observed by transmission electron microscopy (TEM). 175 nM OA for 48 hr was applied to OA modelling induction. Results: Compared to the control group, the OA-induced AD model cells displayed higher levels of p-tau, Aβ42 and β-secretase (P < 0.01), suggesting that the AD model was successfully established. Compared to the OA model group alone, p-tau, Aβ42 and β-secretase levels and autophagy promoter Beclin-1 expression decreased significantly in the BA group (P < 0.05), whereas p-Akt and p-mTOR increased (P < 0.01). Conclusion: BA exhibited a neuroprotection effect against OA-induced cellular injury in the AD model by suppressing the Beclin-1-dependent autophagy pathway, indicating that BA might be an appealing potential strategy to treat AD.