Euodia daniellii Hemsl. (Bee-Bee Tree) Oil Attenuates Palmitate-Induced Lipid Accumulation and Apoptosis in Hepatocytes
- Authors
- Jung, Tae Woo; Kim, Sun-Young; Kim, Da-Som; Shin, Eui-Cheol; Park, Yong Bae; Lee, Kyoung-Tae
- Issue Date
- Apr-2018
- Publisher
- S. Karger AG
- Keywords
- Euodia daniellii Hemsl.; Hepatic lipid accumulation; Apoptosis; Vegetable oil
- Citation
- Pharmacology, v.101, no.5-6, pp 298 - 308
- Pages
- 11
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- Pharmacology
- Volume
- 101
- Number
- 5-6
- Start Page
- 298
- End Page
- 308
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/13148
- DOI
- 10.1159/000487892
- ISSN
- 0031-7012
1423-0313
- Abstract
- Hepatic lipid accumulation and apoptosis is elevated in patients with non-alcoholic steatohepatitis and is closely associated with severity. Saturated fatty acid palmitate stimulates lipid accumulation and apoptosis in hepatocytes. In the present study, we examined bee-bee tree oil (BO)-mediated protective effects on palmitate-induced lipid accumulation and apoptosis in mouse primary hepatocytes. Cells were cultured in a control media or the same media containing 150 or 300 mu mol/L of albumin-bound palmitate for 24 h. BO concentrations used were 0, 0.1, 0.2, or 0.5%. Palmitate induced lipid accumulation and mRNA expression of lipogenic genes such as SREBP1c and SCD1. However, BO prevented these changes. Furthermore, palmitate stimulated caspase-3 activity and decreased cell viability in the absence of BO. BO reduced palmitate-induced activation of caspase-3 and cell death in a dose-dependent manner. AMP-activated protein kinase inhibitors abolished the effects of BO. Furthermore, BO suppressed palmitate-induced c-Jun N-terminal kinase (JNK) phosphorylation through the 5' adenosine monophosphate-activated protein kinase (AMPK)-dependent pathway. In conclusion, BO attenuated palmitate-induced hepatic steatosis and apoptosis through AMPK-mediated suppression of JNK signaling. These data suggest that BO is an important determinant of saturated fatty acid-induced lipid accumulation and apoptosis, and may be an effective therapeutic strategy for treatment of obesity-mediated liver diseases. (C) 2018 S. Karger AG, Basel
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