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Epigallocatechin gallate ameliorates chronic fatigue syndrome in mice: behavioral and biochemical evidence.

Abstract
Three decades after the coining of the term chronic fatigue syndrome, the diagnosis of this illness is still symptom based and the aetiology remains elusive. Chronic fatigue syndrome pathogenesis seems to be multifactorial and the possible involvement of immune system is supported. The present study was designed to evaluate the effects of the epigallocatechin gallate in a mouse model of immunologically induced chronic fatigue. On 19th day, after lipopolysaccharide/Brucella abortus administration, the mice showed significant increase in immobility period, post swim fatigue and thermal hyperalgesia. Behavioral deficits were coupled with enhanced oxidative-nitrosative stress as evident by increased lipid peroxidation, nitrite levels and decreased endogenous antioxidant enzymes (superoxide dismutase, reduced glutathione and catalase) and inflammation (increased levels of tumor necrosis factor-alpha and tissue growth factor-beta). Chronic treatment with epigallocatechin gallate restored these behavioral and biochemical alterations in mice. The present study points out towards the beneficial effect of epigallocatechin gallate in the amelioration of chronic fatigue syndrome and thus may provide a new, effective and powerful strategy to treat chronic fatigue syndrome.
AuthorsAnand Kamal Sachdeva, Anurag Kuhad, Vinod Tiwari, Kanwaljit Chopra
JournalBehavioural brain research (Behav Brain Res) Vol. 205 Issue 2 Pg. 414-20 (Dec 28 2009) ISSN: 1872-7549 [Electronic] Netherlands
PMID19643148 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antioxidants
  • Lipopolysaccharides
  • Nitrites
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Catechin
  • epigallocatechin gallate
  • Catalase
  • Superoxide Dismutase
  • Glutathione
Topics
  • Animals
  • Antioxidants (metabolism, pharmacology)
  • Brucella abortus
  • Catalase (metabolism)
  • Catechin (analogs & derivatives, pharmacology)
  • Disease Models, Animal
  • Fatigue Syndrome, Chronic (chemically induced, drug therapy, metabolism)
  • Glutathione (metabolism)
  • Hyperalgesia (chemically induced, drug therapy)
  • Lipid Peroxidation (drug effects)
  • Lipopolysaccharides
  • Locomotion (drug effects)
  • Mice
  • Mice, Inbred Strains
  • Nitrites (metabolism)
  • Oxidative Stress (drug effects)
  • Superoxide Dismutase (metabolism)
  • Swimming
  • Transforming Growth Factor beta (blood, metabolism)
  • Tumor Necrosis Factor-alpha (blood, metabolism)

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