PMID- 24448843
OWN - NLM
STAT- MEDLINE
DCOM- 20150303
LR  - 20211021
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 37
IP  - 4
DP  - 2014 Aug
TI  - Antihepatotoxic effect of tadehaginoside, extracted from Tadehagi triquetrum 
      (L.), against CCl4-lesioned rats through activating the Nrf2 signaling pathway 
      and attenuating the inflammatory response.
PG  - 1006-14
LID - 10.1007/s10753-014-9821-5 [doi]
AB  - Recently, an increasing number of studies suggest that oxidative stress and 
      inflammation are associated with hepatocellular injuries. Thus, we aimed to 
      evaluate the potential hepatoprotective role of tadehaginoside (TA) on liver 
      lesions induced by carbon tetrachloride (CCl4). The results in vitro suggested 
      that TA dose-dependently suppressed the cell proliferation of HepG2 cells, 
      whereas the phosphorylated level of IkappaBalpha in cells was effectively inactivated. 
      The study in vivo showed that TA significantly lowered the serum concentrations 
      of alanine aminotransferase (ALT), aspartate aminotransferase (AST), 
      immunoglobulin E (IgE), and leukotriene (LT) in CCl4-lesioned rats. Pathological 
      examination indicated that CCl4-induced hepatocellular damage was effectively 
      mitigated by TA treatment. Meanwhile, the contents of gamma-glutamylcysteine 
      synthetase (gamma-GCS), glutathione (GSH), and catalase (CAT) in liver tissue were 
      gradually elevated. In addition, cytochrome c oxidase (COX) mRNA expression in 
      hepatocytes was markedly upregulated, and nuclear factor E2-related factor 2 
      (Nrf2) and Kelch-like ECH-associated protein 1 (Keapl) levels were progressively 
      increased. Furthermore, the tumor necrosis factor alpha (TNF-alpha) and nuclear 
      factor-kappa B (NF-kappaB)-expressed protein were downregulated. These findings 
      demonstrate that tadehaginoside effectively protects against CCl4-induced 
      oxidative injury and inflammatory reaction in hepatocytes, in which the 
      underlying mechanisms are involved in activating the Nrf2 signaling pathway and 
      inhibiting the NF-kappaB pathway, thereby attenuating oxidative stress and reducing 
      the inflammation in liver cells.
FAU - Tang, Aicun
AU  - Tang A
AD  - The First Affiliated Hospital of Guangxi University of Chinese Medicine, No. 89 
      Dongge Road, Nanning City, Guangxi, 530023, People's Republic of China.
FAU - Chen, Xiaoyu
AU  - Chen X
FAU - Lu, Qiuyu
AU  - Lu Q
FAU - Zheng, Ni
AU  - Zheng N
FAU - Wei, Yanfei
AU  - Wei Y
FAU - Wu, Xiaoyan
AU  - Wu X
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Coumaric Acids)
RN  - 0 (Glucosides)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (KEAP1 protein, rat)
RN  - 0 (Kelch-Like ECH-Associated Protein 1)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Nfe2l2 protein, rat)
RN  - 0 (Plant Extracts)
RN  - 0 (RNA, Messenger)
RN  - 0 (tadehaginoside)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - CL2T97X0V0 (Carbon Tetrachloride)
SB  - IM
MH  - Animals
MH  - Carbon Tetrachloride/toxicity
MH  - Chemical and Drug Induced Liver Injury/*drug therapy/metabolism
MH  - Coumaric Acids/chemistry/*pharmacology
MH  - Fabaceae/*chemistry
MH  - Gene Expression Regulation/drug effects
MH  - Glucosides/chemistry/*pharmacology
MH  - Hep G2 Cells
MH  - Humans
MH  - Immunoglobulin E/immunology
MH  - Inflammation/drug therapy/metabolism
MH  - Intracellular Signaling Peptides and Proteins/metabolism
MH  - Kelch-Like ECH-Associated Protein 1
MH  - Liver/*drug effects/pathology
MH  - Male
MH  - Models, Chemical
MH  - NF-E2-Related Factor 2/*metabolism
MH  - Oxidative Stress
MH  - Phosphorylation
MH  - Plant Extracts/chemistry/*pharmacology
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Signal Transduction
EDAT- 2014/01/23 06:00
MHDA- 2015/03/04 06:00
CRDT- 2014/01/23 06:00
PHST- 2014/01/23 06:00 [entrez]
PHST- 2014/01/23 06:00 [pubmed]
PHST- 2015/03/04 06:00 [medline]
AID - 10.1007/s10753-014-9821-5 [doi]
PST - ppublish
SO  - Inflammation. 2014 Aug;37(4):1006-14. doi: 10.1007/s10753-014-9821-5.