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Measurements of Physiological Stress Responses in C. Elegans
Published on: May 21, 2020
Integrated quantitative proteomics reveals stress-associated network remodeling induced by mitragynine in RSC96
Hasriadi Hasriadi1,2, Dasuni Wasana Peththa Wadu3, Thorsang Weerakul4
1Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, 10330, Thailand.
Archives of Toxicology
|July 9, 2026
Summary
Chronic kratom (Mitragyna speciosa) exposure alters Schwann cells, impacting cellular functions and potentially leading to neurotoxicity. This study reveals molecular changes linked to tolerance and risk.
Area of Science:
- Neuroscience
- Proteomics
- Cell Biology
Background:
- Mitragynine, kratom's main alkaloid, offers pain relief but causes tolerance.
- Schwann cells are vulnerable to toxins, and their dysfunction links to neurotoxicity.
- Mechanisms of kratom's cellular adaptation are not well understood.
Purpose of the Study:
- To investigate molecular changes in Schwann cells due to mitragynine exposure.
- To understand the cellular mechanisms behind mitragynine tolerance and neurotoxic potential.
Main Methods:
- Quantitative proteomics (LC-MS/MS) and systems biology on RSC96 Schwann cells exposed to mitragynine.
- Bioinformatic analyses including pathway mapping (GO, KEGG, Reactome) and network reconstruction (STRING, BioGRID).
Main Results:
- Identified 91 differentially expressed proteins (60 down, 31 up) after 72h exposure to 20 µM mitragynine.
- Observed suppressed translational machinery, cytoskeleton, and metabolic pathways.
- Highlighted AMP-activated protein kinase (AMPK) as a key downregulated node; upregulated proteins involved in stress response and chromatin remodeling.
Conclusions:
- Chronic mitragynine exposure induces significant proteomic remodeling in Schwann cells.
- Observed changes suggest adaptive responses related to tolerance and potential peripheral neurotoxic risk.
- Limited structural similarity between mitragynine and morphine suggests distinct mechanisms despite shared targets.
