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Reduction of emodin-8-O-ß-D-glucoside content participates in processing-based detoxification of polygoni multiflori
Xu Wang1, Guode Zhao1, Chengguo Ju2
1Wuya College of Innovation, Shenyang Pharmaceutical University, No. 103, Wenhua Roa, Shenyang, Liaoning 110016, PR China.
Background:
The occurrence of severe liver injury by the herbal medicine Polygoni Multiflori Radix (PMR) has drawn significant attention. The fact that processing attenuates PMR-induced hepatotoxicity has been well accepted, but the mechanisms are still ambiguous.
Purpose:
This study aimed to illuminate the mechanism of processing-based attenuation of PMR hepatotoxicity.
Methods:
The contents of emodin-8-O-β-d-glucoside (EG) and emodin (EMD) in raw and processed PMR were quantified. The difference in toxicokinetic behaviors of EG and EMD was determined in vivo, and the disposition properties of EG were investigated in vitro and in vivo.
Results:
Decreased EG content was found in processed (black bean) PMR. Processed PMR showed reduced adverse effects relative to raw PMR. In addition, less hepatic protein adduction derived from EMD was produced in mice after exposure to processed PMR than that in animals receiving raw PMR. Glucose transporters SGLT1 and GLUT2 participated in the absorption of EG, and effective hydrolysis of EG to EMD took place in the intestinal epithelial cells during the process of absorption. Cytosolic broad-specificity β-glucosidase and lactase phlorizin hydrolase, as well as intestinal flora, participated in the hydrolysis of EG. The circulated EMD resulting from the deglycosylation of EG executed the hepatotoxic action.
Conclusion:
EG is a pre-toxin and can be metabolically activated to EMD participating in the hepatotoxic event. The reduction of EG content due to processing is a key mechanistic factor that initiates the detoxification of PMR.
Insights
Processing Polygoni Multiflori Radix (PMR) reduces liver injury by decreasing emodin-8-O-β-d-glucoside (EG), a pre-toxin. This processing detoxifies PMR by limiting its conversion to the toxic compound emodin (EMD).
Area of Science:
- Pharmacology
- Toxicology
- Herbal Medicine Research
Background:
- Severe liver injury associated with Polygoni Multiflori Radix (PMR) is a significant concern.
- Processing is known to reduce PMR-induced hepatotoxicity, but the underlying mechanisms remain unclear.
Purpose of the Study:
- To elucidate the mechanism by which processing attenuates hepatotoxicity induced by Polygoni Multiflori Radix.
- To investigate the role of specific compounds and their metabolic pathways in PMR hepatotoxicity.
Main Methods:
- Quantification of emodin-8-O-β-d-glucoside (EG) and emodin (EMD) in raw and processed PMR.
- In vivo and in vitro investigation of toxicokinetic behaviors and disposition properties of EG and EMD.
- Analysis of hepatic protein adduction and involvement of glucose transporters (SGLT1, GLUT2) and enzymes in EG metabolism.
Main Results:
- Processed PMR exhibited significantly lower EG content and reduced hepatotoxicity compared to raw PMR.
- EG is absorbed via glucose transporters SGLT1 and GLUT2 and effectively hydrolyzed to EMD in intestinal epithelial cells.
- EMD, derived from EG deglycosylation by enzymes and intestinal flora, is responsible for the hepatotoxic action.
Conclusions:
- Emodin-8-O-β-d-glucoside (EG) acts as a pre-toxin, metabolically activated to emodin (EMD), which mediates hepatotoxicity.
- Reduced EG content in processed PMR is the primary mechanism for its detoxification.
- Understanding these metabolic pathways is crucial for the safe use of PMR.
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