PMID- 29864915
OWN - NLM
STAT- MEDLINE
DCOM- 20181011
LR  - 20181011
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 103
DP  - 2018 Jul
TI  - Dihydrocurcumin ameliorates the lipid accumulation, oxidative stress and insulin 
      resistance in oleic acid-induced L02 and HepG2 cells.
PG  - 1327-1336
LID - S0753-3322(18)31509-9 [pii]
LID - 10.1016/j.biopha.2018.04.143 [doi]
AB  - AIMS: Curcumin is a polyphenol compound with many pharmacological activities 
      including antioxidant, lipid-loweing and liver protective. Dihydrocurcumin (DHC) 
      is one of the major metabolites of curcumin. So far, the pharmacological activity 
      of DHC has not been reported. Here, we evaluate the effects of DHC on oleic acid 
      (OA)-induced lipid accumulation, oxidative stress and insulin resistance and the 
      underlying mechanism in L02 and HepG2 cells. MAIN METHODS: OA-induced L02 and 
      HepG2 cells were used as the in vitro model of nonalcoholic fatty liver disease 
      (NAFLD). Lipid accumulation, oxidative stress, glucose uptake and cell 
      inflammation were evaluated by cellular biochemical assay, respectively. 
      Signaling pathways involved in lipid metabolism including peroxisome proliferator 
      activated receptor-alpha (PPARalpha), the sterol regulatory element binding protein-1C 
      (SREBP-1C) and patatin-like phospholipase domain containing 3 (PNPLA3), glucose 
      uptake including phosphatidylinositol 3-kinase (PI3K) and phosphorylated 
      serine-threonine protein kinase (pAKT), and oxidative stress including nuclear 
      factor E2-related factor 2 (Nrf2), cytochrome P450 4A (CYP4A) and 2E1 (CYP2E1) 
      were investigated by western blotting and RT-qPCR, respectively. KEY FINDINGS: 
      DHC decreased the levels of cellular triglycerides (TG) by regulating the mRNA 
      and protein expression levels of SREBP-1C, PNPLA3 and PPARalpha. At the same time, 
      DHC improved the hepatocellular glucose uptake by increasing the protein 
      expression levels of pAKT and PI3K. Furthermore, DHC reduced the levels of 
      cellular NO and ROS via Nrf2 signaling pathways. SIGNIFICANCE: The present study 
      firstly revealed that DHC ameliorated OA-induced steatosis through regulating the 
      lipid metabolism, oxidative stress and insulin resistance in HepG2 and L02 cells.
CI  - Copyright (c) 2018 Elsevier Masson SAS. All rights reserved.
FAU - Yu, Qingqing
AU  - Yu Q
AD  - Hubei Province Key Laboratory of Biotechnology of Chinese Traditional Medicine, 
      National & Local Joint Engineering Research Center of High-throughput Drug 
      Screening Technology, Hubei University, Wuhan Hubei 430062, PR China.
FAU - Liu, Yayun
AU  - Liu Y
AD  - Hubei Province Key Laboratory of Biotechnology of Chinese Traditional Medicine, 
      National & Local Joint Engineering Research Center of High-throughput Drug 
      Screening Technology, Hubei University, Wuhan Hubei 430062, PR China.
FAU - Wu, Yufei
AU  - Wu Y
AD  - Hubei Province Key Laboratory of Biotechnology of Chinese Traditional Medicine, 
      National & Local Joint Engineering Research Center of High-throughput Drug 
      Screening Technology, Hubei University, Wuhan Hubei 430062, PR China.
FAU - Chen, Yong
AU  - Chen Y
AD  - Hubei Province Key Laboratory of Biotechnology of Chinese Traditional Medicine, 
      National & Local Joint Engineering Research Center of High-throughput Drug 
      Screening Technology, Hubei University, Wuhan Hubei 430062, PR China. Electronic 
      address: cy101610@qq.com.
LA  - eng
PT  - Journal Article
DEP - 20180507
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Triglycerides)
RN  - 2UMI9U37CP (Oleic Acid)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - IT942ZTH98 (Curcumin)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Cell Death/drug effects
MH  - Cell Survival/drug effects
MH  - Curcumin/chemistry/*pharmacology
MH  - Gene Expression Regulation/drug effects
MH  - Glucose/metabolism
MH  - Hep G2 Cells
MH  - Humans
MH  - Inflammation/pathology
MH  - *Insulin Resistance
MH  - Lipid Metabolism/*drug effects
MH  - Nitric Oxide/metabolism
MH  - Oleic Acid/*pharmacology
MH  - Oxidative Stress/*drug effects
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Phosphorylation/drug effects
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/drug effects
MH  - Triglycerides/metabolism
OTO - NOTNLM
OT  - Dihydrocurcumin
OT  - Insulin resistance
OT  - Lipid metabolism
OT  - NAFLD
OT  - Oxidative stress
EDAT- 2018/06/06 06:00
MHDA- 2018/10/12 06:00
CRDT- 2018/06/06 06:00
PHST- 2018/03/08 00:00 [received]
PHST- 2018/04/18 00:00 [revised]
PHST- 2018/04/18 00:00 [accepted]
PHST- 2018/06/06 06:00 [entrez]
PHST- 2018/06/06 06:00 [pubmed]
PHST- 2018/10/12 06:00 [medline]
AID - S0753-3322(18)31509-9 [pii]
AID - 10.1016/j.biopha.2018.04.143 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2018 Jul;103:1327-1336. doi: 10.1016/j.biopha.2018.04.143. 
      Epub 2018 May 7.