Carnosic acid attenuates inflammation, oxidative stress and mitochondrial dysfunction in neurons via activation of AMPK/SIRT1 pathway

Purpose: To determine the effects and mechanism of action of carnosic acid (CA), a natural diterpenoid compound, on the neuroprotective roles of anesthetics.Methods: The effects of carnosic acid (CA) on cell viability and apoptosis were evaluated by MTT assay and flow cytometry, respectively. Its effects on mitochondrial damage was assessed by JC-1 staining, while oxidative stress and inflammatory response were determined by enzyme-linked immunosorbent assay (ELISA) and immunoblot assays, respectively. Immunoblot assays were performed to evaluate the effect of CA on AMPK/SIRT1 pathway. Results: Carnosic acid (CA) increased the survival rate of isoflurane-induced neuronal cells, but inhibited isoflurane-induced mitochondrial damage in neurons (p < 0.01). CA also suppressed isoflurane-induced oxidative stress in neurons, and inhibited isoflurane-induced neuronal inflammatory response (p < 0.01). Furthermore, CA activated AMPK/SIRT1 pathway, and also attenuated inflammation, oxidative stress and mitochondrial dysfunction in neurons induced by isoflurane (p < 0.01).Conclusion: Carnosic acid attenuates inflammation, oxidative stress and mitochondrial dysfunction in neurons via activation of AMPK/SIRT1 pathway. Thus, it has potentials for use in the treatment of neurotoxicity

Automated summary

This study found that carnosic acid can attenuate inflammation, oxidative stress and mitochondrial dysfunction in neurons via activation of the AMPK/SIRT1 pathway.