Ou Liao1,
Keqi Xie2 
,
Xianjie Zhang1,
Wencai Jiang1,
Wen Li1,
An Xie1
For correspondence:- Keqi Xie Email: x_keqi0801@163.com Tel:+8615808160448
Accepted: 11 October 2022 Published: 30 November 2022
Citation: Liao O, Xie K, Zhang X, Jiang W, Li W, Xie A. Carnosic acid attenuates inflammation, oxidative stress and mitochondrial dysfunction in neurons via activation of AMPK/SIRT1 pathway. Trop J Pharm Res 2022; 21(11):2359-2365 doi: 10.4314/tjpr.v21i11.13
© 2022 The authors.
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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
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