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Application of iTRAQ-Based Quantitative Proteomics Approach to Identify Deregulated Proteins Associated with Liver
Longfei Lin1, Hui Li1, Hongmei Lin2
1Institute Chinese materia medica china academy of Chinese medical sciences, Beijing, China.
Background/Aims:
Clinical reports on adverse reactions that result from Polygonum multiflorum (PM) and its preparations, especially regarding liver injury, have recently received widespread attention. This study aimed to investigate the mechanism of hepatotoxicity induced by different PM extracts through iTRAQ quantitative proteomics.
Methods:
The different PM extracts were orally administrated for 90 days to rats, and the hepatotoxicity effect was evaluated through measurement of biochemical indexes, oxidative damage indexes and hematoxylin-eosin (HE) staining. Then, the hepatotoxicity mechanism was investigated by iTRAQ quantitative proteomics.
Results:
The results of biochemical and histopathological analyses showed that liver injury occurred in all groups of rats given by various PM extracts, which proved all of the PM extracts could induce hepatotoxicity. The hepatotoxicity mechanism may differ between the total extract group and the other groups through the results of biochemical indicators. The iTRAQ proteomics study showed that hepatotoxicity resulting from PM was mainly related to the abnormal activity of mitochondrion function-related oxidative phosphorylation pathways.
Conclusion:
This iTRAQ proteomics study revealed that the hepatotoxicity induced by PM is primarily related to the oxidative phosphorylation pathways. NADH dehydrogenase family proteins and Slc16a2 could be potential biomarkers of hepatotoxicity resulting from PM.
Insights
Polygonum multiflorum (PM) extracts cause liver injury by disrupting mitochondrial oxidative phosphorylation. NADH dehydrogenase and Slc16a2 may serve as biomarkers for PM-induced hepatotoxicity.
Area of Science:
- Pharmacology
- Toxicology
- Proteomics
Background:
- Clinical reports highlight adverse reactions from Polygonum multiflorum (PM) preparations, particularly liver injury.
- Understanding the mechanism of PM-induced hepatotoxicity is crucial due to widespread attention.
Purpose of the Study:
- To investigate the mechanism of hepatotoxicity induced by different PM extracts.
- To utilize iTRAQ quantitative proteomics to elucidate PM's toxicological pathways.
Main Methods:
- Oral administration of various PM extracts to rats for 90 days.
- Evaluation of hepatotoxicity via biochemical indexes, oxidative damage markers, and HE staining.
- Application of iTRAQ quantitative proteomics to identify molecular mechanisms.
Main Results:
- All PM extracts induced significant liver injury in rats, confirmed by biochemical and histopathological analyses.
- Hepatotoxicity mechanisms may vary between total extract and other PM extract groups.
- iTRAQ proteomics revealed PM-induced hepatotoxicity is linked to abnormal mitochondrial oxidative phosphorylation pathways.
Conclusions:
- PM-induced hepatotoxicity is primarily associated with disruptions in oxidative phosphorylation pathways.
- NADH dehydrogenase family proteins and Slc16a2 are identified as potential biomarkers for PM-induced liver injury.
