PMID- 15925388
OWN - NLM
STAT- MEDLINE
DCOM- 20050929
LR  - 20131121
IS  - 0024-3205 (Print)
IS  - 0024-3205 (Linking)
VI  - 77
IP  - 15
DP  - 2005 Aug 26
TI  - Melatonin ameliorates carbon tetrachloride-induced hepatic fibrogenesis in rats 
      via inhibition of oxidative stress.
PG  - 1902-15
AB  - Melatonin is reported to exhibit a wide variety of biological effects, including 
      antioxidant and anti-inflammatory. Evidence shows the important role of oxidative 
      stress in the etiopathogenesis of hepatic fibrosis. The aim of this study was to 
      investigate the protective effects of administration of melatonin in rats with 
      carbon tetrachloride-induced fibrosis for 6 weeks. Hepatic fibrotic changes were 
      evaluated biochemically by measuring tissue hydroxyproline levels and 
      histopathogical examinations. Malondialdehyde (MDA), an end product of lipid 
      peroxidation, and glutathione peroxidase (GSH-px) and superoxide dismutase (SOD) 
      levels were evaluated in tissue homogenates by spectrophotometry. The nuclear 
      factor-kappaB (NF-kappaB) in liver tissue was examined by immunohistochemistry. 
      Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) 
      concentrations in Kupffer cells (KCs) culture supernatants were measured with 
      ELISA. The rats injected subcutaneously with CCl4 for 6 weeks resulted in hepatic 
      fibrotic changes increased hydroxyproline and MDA levels, and decreased GSH-px 
      and SOD levels, whereas melatonin reversed these effects. Furthermore, melatonin 
      inhibited the expression of NF-kappaB in liver tissue and decreasing production 
      of proinflammatory cytokines such as TNF-alpha and IL-1beta from KCs in fibrotic 
      rats. These present results suggest that melatonin ameliorates carbon 
      tetrachloride-induced hepatic fibrogenesis in rats via inhibition of oxidative 
      stress and proinflammatory cytokines production.
FAU - Wang, Hua
AU  - Wang H
AD  - Institute of Clinical Pharmacology, Anhui Medical University, Hefei 230032, 
      China. wanghua@ahmu.edu.cn
FAU - Wei, Wei
AU  - Wei W
FAU - Wang, Ni-Ping
AU  - Wang NP
FAU - Gui, Shuang-Yin
AU  - Gui SY
FAU - Wu, Li
AU  - Wu L
FAU - Sun, Wu-Yi
AU  - Sun WY
FAU - Xu, Shu-Yun
AU  - Xu SY
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Serum Albumin)
RN  - 0 (Serum Globulins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - CL2T97X0V0 (Carbon Tetrachloride)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - EC 2.6.1.1 (Aspartate Aminotransferases)
RN  - EC 2.6.1.2 (Alanine Transaminase)
RN  - JL5DK93RCL (Melatonin)
RN  - RMB44WO89X (Hydroxyproline)
SB  - IM
MH  - Alanine Transaminase/blood
MH  - Animals
MH  - Aspartate Aminotransferases/blood
MH  - Carbon Tetrachloride
MH  - Glutathione Peroxidase/metabolism
MH  - Hydroxyproline/metabolism
MH  - Interleukin-1/metabolism
MH  - Kupffer Cells/drug effects/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Liver/drug effects/metabolism/pathology
MH  - Liver Cirrhosis, Experimental/chemically induced/pathology/*prevention & control
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Melatonin/*pharmacology
MH  - NF-kappa B/metabolism
MH  - Oxidative Stress/*drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Serum Albumin/metabolism
MH  - Serum Globulins/metabolism
MH  - Superoxide Dismutase/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2005/06/01 09:00
MHDA- 2005/09/30 09:00
CRDT- 2005/06/01 09:00
PHST- 2004/10/29 00:00 [received]
PHST- 2005/04/15 00:00 [accepted]
PHST- 2005/06/01 09:00 [pubmed]
PHST- 2005/09/30 09:00 [medline]
PHST- 2005/06/01 09:00 [entrez]
AID - S0024-3205(05)00407-8 [pii]
AID - 10.1016/j.lfs.2005.04.013 [doi]
PST - ppublish
SO  - Life Sci. 2005 Aug 26;77(15):1902-15. doi: 10.1016/j.lfs.2005.04.013.