PMID- 15902742
OWN - NLM
STAT- MEDLINE
DCOM- 20050628
LR  - 20190430
IS  - 1007-9327 (Print)
IS  - 2219-2840 (Electronic)
IS  - 1007-9327 (Linking)
VI  - 11
IP  - 19
DP  - 2005 May 21
TI  - Protective effect of fufanghuangqiduogan against acute liver injury in mice.
PG  - 2984-9
AB  - AIM: To study the effects and possible mechanisms of fufanghuangqiduogan (FFHQ) 
      in mice with acute liver injury (ALI). METHODS: ALI was successfully induced by 
      injecting carbon tetrachloride (CCl4) intraperitoneally and by tail vein 
      injection of Bacillus Calmette Guerin (BCG) and lipopolysaccharide (LPS) in mice, 
      respectively. Each of the two model groups was divided into normal group, model 
      group, FFHQ (60, 120 and 240 mg/kg) treatment groups, and bifendate treatment 
      group. At the end of the experiment, levels of alanine aminotransferase (ALT) and 
      aspartate aminotransferase (AST), content of malondialdehyde (MDA), activities of 
      superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) in liver 
      homogenate were measured by biochemical methods. The activities of tumor necrosis 
      factor-alpha (TNF-alpha) and interleukin-1 (IL-1) were determined by 
      radio-immunoassay. Hepatic tissue sections were stained with hematoxylin and 
      eosin and examined under a light microscope. RESULTS: In the two models of ALI, 
      FFHQ (60, 120, 240 mg/kg) was found to significantly decrease the serum 
      transaminase (ALT, AST) activities. Meanwhile, FFHQ decreased MDA contents and 
      upregulated the lower SOD and GSH-px levels in liver homogenate. Furthermore, in 
      immunologic liver injury model, FFHQ decreased levels of TNF-alpha and IL-1 in 
      serum. Histologic examination showed that FFHQ could attenuate the area and 
      extent of necrosis, reduce the immigration of inflammatory cells. CONCLUSION: 
      FFHQ had protective effect on liver injury induced by either CCl4 or BCG+LPS in 
      mice, and its mechanisms were related to free radical scavenging, increasing SOD 
      and GSH-px activities and inhibiting the production of proinflammatory mediators.
FAU - Gui, Shuang-Ying
AU  - Gui SY
AD  - Institute of Clinical Pharmacology, Anhui Medical University, Hefei 230032, Anhui 
      Province, China.
FAU - Wei, Wei
AU  - Wei W
FAU - Wang, Hua
AU  - Wang H
FAU - Wu, Li
AU  - Wu L
FAU - Sun, Wu-Yi
AU  - Sun WY
FAU - Wu, Cheng-Yi
AU  - Wu CY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 0 (Drugs, Chinese Herbal)
RN  - 0 (Lipopolysaccharides)
RN  - CL2T97X0V0 (Carbon Tetrachloride)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Carbon Tetrachloride
MH  - Chemical and Drug Induced Liver Injury/*drug therapy/pathology
MH  - Disease Models, Animal
MH  - Drugs, Chinese Herbal/*pharmacology
MH  - Lipopolysaccharides
MH  - Liver/enzymology/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Mycobacterium bovis
PMC - PMC4305673
EDAT- 2005/05/20 09:00
MHDA- 2005/06/29 09:00
PMCR- 2005/05/21
CRDT- 2005/05/20 09:00
PHST- 2005/05/20 09:00 [pubmed]
PHST- 2005/06/29 09:00 [medline]
PHST- 2005/05/20 09:00 [entrez]
PHST- 2005/05/21 00:00 [pmc-release]
AID - 10.3748/wjg.v11.i19.2984 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2005 May 21;11(19):2984-9. doi: 10.3748/wjg.v11.i19.2984.