4.7 Article

Reduction of emodin-8-O-β-D-glucoside content participates in processing-based detoxification of polygoni multiflori radix

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PHYTOMEDICINE
卷 114, 期 -, 页码 -

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ELSEVIER GMBH
DOI: 10.1016/j.phymed.2023.154750

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Polygoni multiflori radix; Hepatotoxicity; Processing detoxification; Emodin-8-O-beta-D-glucoside

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This study aimed to elucidate the mechanism underlying the reduced hepatotoxicity of Polygoni Multiflori Radix (PMR) after processing. It was found that processed PMR contained lower levels of emodin-8-O-beta-D-glucoside (EG). Processed PMR showed fewer adverse effects and less hepatic protein adduction compared to raw PMR. Effective hydrolysis of EG to emodin (EMD) occurred in the intestinal epithelial cells during absorption. Cytosolic broad-specificity beta-glucosidase, lactase phlorizin hydrolase, and intestinal flora participated in the hydrolysis of EG. Circulating EMD resulting from the deglycosylation of EG exerted hepatotoxic effects. The reduction of EG content due to processing is a key factor in the detoxification of PMR.
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-beta-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 beta-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.

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