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Hepatoprotective effects of kaempferol 3-O-rutinoside and kaempferol 3-O-glucoside from Carthamus tinctorius L. on CCl(4)-induced oxidative liver injury in mice

Safflower (Carthamus tinctorius L.) is a traditional medicinal and edible herb with a long history of use in China. In this study, a model of hepatotoxicity induced by carbon tetrachloride (CCl(4)) in mice was used to investigate the hepatoprotective effects of kaempferol 3-O-rutinoside (K-3-R) and...

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Detalles Bibliográficos
Autores principales: Wang, Yu, Tang, Changyun, Zhang, Hao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taiwan Food and Drug Administration 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9351762/
https://www.ncbi.nlm.nih.gov/pubmed/28911387
http://dx.doi.org/10.1016/j.jfda.2014.10.002
Descripción
Sumario:Safflower (Carthamus tinctorius L.) is a traditional medicinal and edible herb with a long history of use in China. In this study, a model of hepatotoxicity induced by carbon tetrachloride (CCl(4)) in mice was used to investigate the hepatoprotective effects of kaempferol 3-O-rutinoside (K-3-R) and kaempferol 3-O-glucoside (K-3-G), two kaempferol glycosides isolated from C. tinctorius L. K-3-R and K-3-G, at doses of 200 mg/kg and 400 mg/kg, were given orally to male mice once/d for 7 days before they received CCl(4) intraperitoneally. Our results showed that K-3-R and K-3-G treatment increased the level of total protein (TP) and prevented the CCl(4)-induced increases in serum aspartate aminotransferase (AST), serum alkaline phosphatase (ALP), and hepatic malondialdehyde (MDA) levels. Additionally, mice treated with K-3-R and K-3-G had significantly restored glutathione (GSH) levels and showed normal catalase (CAT) and superoxide dismutase (SOD) activities, compared to CCl(4)-treated mice. K-3-R and K-3-G also mitigated the CCl(4)-induced liver histological alteration, as indicated by histopathological evaluation. These findings demonstrate that K-3-R and K-3-G have protective effects against acute CCl(4)-induced oxidative liver damage.