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Published on: April 24, 2021
Arctigenin alleviates ER stress via activating AMPK
Yuan Gu1, Xiao-xiao Sun, Ji-ming Ye
1Department of Tumor Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, China.
Acta Pharmacologica Sinica
|June 19, 2012
Summary
Arctigenin (ATG) protects cells from endoplasmic reticulum (ER) stress by activating AMP-activated protein kinase (AMPK). This activation reduces protein synthesis and ER load, offering a potential therapeutic strategy for ER-related diseases.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Endoplasmic reticulum (ER) stress is implicated in various diseases.
- Identifying novel regulators of ER stress is crucial for therapeutic development.
Purpose of the Study:
- To investigate the protective effects of arctigenin (ATG) against ER stress.
- To elucidate the underlying mechanisms of ATG's action.
Main Methods:
- Cell-based screening assays and MTT assays for viability.
- Gene and protein expression analysis via PCR and Western blotting.
- RNA interference (RNAi) for gene silencing and ATP level measurements.
Main Results:
- Arctigenin inhibited cell death and unfolded protein response (UPR) induced by brefeldin A in a dose-dependent manner.
- ATG attenuated protein synthesis by inhibiting mTOR-p70S6K signaling and eEF2 activity, partially reversed by AMPKα1 silencing.
- ATG activated AMP-activated protein kinase (AMPK) by reducing intracellular ATP levels and inhibiting mitochondrial complex I respiration.
Conclusions:
- Arctigenin acts as an effective ER stress alleviator.
- ATG protects cells against ER stress by activating AMPK.
- AMPK activation by ATG leads to attenuated protein translation and reduced ER load.
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