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Humulus japonicus Extracts Protect Against Lipopolysaccharide/d-Galactosamine-Induced Acute Liver Injury in Rats

Authors
Bae, JinhyungMin, Young SilNam, YoonjinLee, Hyun SeokSohn, Uy Dong
Issue Date
Oct-2018
Publisher
MARY ANN LIEBERT, INC
Keywords
antioxidative; hepatotoxicity; Humulus japonicus; liver
Citation
JOURNAL OF MEDICINAL FOOD, v.21, no.10, pp 1009 - 1015
Pages
7
Journal Title
JOURNAL OF MEDICINAL FOOD
Volume
21
Number
10
Start Page
1009
End Page
1015
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/736
DOI
10.1089/jmf.2018.4178
ISSN
1096-620X
1557-7600
Abstract
It has been described that Humulus japonicus has potential antituberculosis and anti-inflammatory effects. The antiaging activity of H. japonicus extract (HJE) was also examined not only in yeast but also in human fibroblast cells. We evaluated the protective effect of HJE on hepatotoxicity in this study. We demonstrated the expression of antioxidative enzyme and cytokines in plasma. The vehicle control group received orally administered normal saline. Acute hepatotoxicity rat model was induced by lipopolysaccharide (LPS) (30g/kg) and d-galactosamine (D-GalN) (500mg/kg) by intraperitoneal injection. The positive control group received orally administered silymarin (10mg/kg). Three HJE groups received 8, 16, and 32mg/kg. The blood samples were prepared to evaluate malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) level to examine oxidative stress, and hepatic tissue was assayed for myeloperoxidase (MPO). Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor- (TNF-) activities were also assayed to examine liver cell viability. Pretreatment with HJE decreased levels of AST, ALT, MDA, MPO, and TNF- and increased levels of SOD and CAT compared with the LPS/D-GalN-treated group. These results suggested that HJE has the potential to reduce oxidative damage and inflammatory reactions in LPS/D-GalN-induced liver injury in the rat model. It can also increase survival rate in LPS/D-GalN-induced hepatotoxicity rat models.
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