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1.
Journal of Integrative Medicine ; (12): 289-301, 2023.
Artigo em Inglês | WPRIM | ID: wpr-982679

RESUMO

OBJECTIVE@#Recent investigations have demonstrated that Polygonum perfoliatum L. can protect against chemical liver injury, but the mechanism behind its efficacy is still unclear. Therefore, we studied the pharmacological mechanism at work in P. perfoliatum protection against chemical liver injury.@*METHODS@#To evaluate the activity of P. perfoliatum against chemical liver injury, levels of alanine transaminase, lactic dehydrogenase, aspartate transaminase, superoxide dismutase, glutathione peroxidase and malondialdehyde were measured, alongside histological assessments of the liver, heart and kidney tissue. A nontargeted lipidomics strategy based on ultra-performance liquid chromatography quadrupole-orbitrap high-resolution mass spectrometry method was used to obtain the lipid profiles of mice with chemical liver injury and following treatment with P. perfoliatum; these profiles were used to understand the possible mechanisms behind P. perfoliatum's protective activity.@*RESULTS@#Lipidomic studies indicated that P. perfoliatum protected against chemical liver injury, and the results were consistent between histological and physiological analyses. By comparing the profiles of liver lipids in model and control mice, we found that the levels of 89 lipids were significantly changed. In animals receiving P. perfoliatum treatment, the levels of 8 lipids were significantly improved, relative to the model animals. The results showed that P. perfoliatum extract could effectively reverse the chemical liver injury and significantly improve the abnormal liver lipid metabolism of mice with chemical liver injury, especially glycerophospholipid metabolism.@*CONCLUSION@#Regulation of enzyme activity related to the glycerophospholipid metabolism pathway may be involved in the mechanism of P. perfoliatum's protection against liver injury. Please cite this article as: Peng L, Chen HG, Zhou X. Lipidomic investigation of the protective effects of Polygonum perfoliatum against chemical liver injury in mice. J Integr Med. 2023; 21(3): 289-301.


Assuntos
Animais , Camundongos , Polygonum/química , Lipidômica , Fígado , Lipídeos/farmacologia , Glicerofosfolipídeos/farmacologia , Doença Hepática Induzida por Substâncias e Drogas/metabolismo
2.
Chinese Pharmacological Bulletin ; (12): 1303-1308, 2017.
Artigo em Chinês | WPRIM | ID: wpr-614196

RESUMO

Aim Based on the effect of total flavonoids extracted from Polygonum perfoliatum L.(TFP) against dimethylnitrosamine(DMN)-induced hepatic fibrosis(HF), to investigate the anti-fibrotic mechanism of TFP.Methods Ninety SD rats were divided into normal group, model group, colchicines(0.1 mg·kg-1) group, and TFP(200, 100, 50 mg·kg-1) group.Except the rats of normal group, other rats were injected intraperitoneally with volume fraction 0.5% DMN solution(2 mL·kg-1) for eight weeks, once every two days.From the first day of modeling, each administration group was given the corresponding dose of drugs to intervene, and the normal group and model group were given an equal volume of solvent, once a day.At the end of the eighth week, the blood and liver tissues were collected.Liver tissue was taken at a fixed position, and the degree of liver tissue was observed by HE staining.The contents of serum ALT, AST, SOD and MDA were measured using colorimetric method;the levels of serum HA, LN, PCⅢand Ⅳ-C were detected using enzyme-linked immunosorbent assay(ELISA);the levels of TNF-α, IL-1β and IL-6 in liver tissues were detected by ELISA;the expression of α-SMA, TGF-β1, p-JAK2 and p-STAT3 were detected by Western blot.Results Compared with the model group, TFP(200, 100, 50 mg·kg-1) could improve the liver tissue lesions, reduce the expression of ALT, AST, HA, LN, PCⅢ, IV-C and MDA, increase SOD activity, reduce the levels of TNF-α, IL-1β and IL-6, and inhibit the expression of α-SMA, TGF-β1, JAK2, STAT3, p-JAK2 and p-STAT3.Conclusion TFP could inhibit DMN-induced HF of rats, which may be involved with antioxidant and inhibiting expression of TGF-β1, JAK2/STAT3 signaling pathway and inflammatory response.

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