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

被引:27
作者
Sachdeva, Anand Kamal [1 ]
Kuhad, Anurag [1 ]
Tiwari, Vinod [1 ]
Chopra, Kanwaljit [1 ]
机构
[1] Panjab Univ, UGC Ctr Adv Study, Univ Inst Pharmaceut Sci, Pharmacol Res Lab, Chandigarh 160014, India
关键词
Chronic fatigue syndrome; Epigallocatechin gallate; Lipopolysaccharide; Brucella abortus; Tumor necrosis factor-alpha; TUMOR-NECROSIS-FACTOR; NITRIC-OXIDE SYNTHASE; FACTOR-KAPPA-B; GENE-EXPRESSION; CYTOKINE PRODUCTION; HUMAN CHONDROCYTES; OXIDATIVE STRESS; MURINE MODEL; FACTOR-ALPHA; IN-VITRO;
D O I
10.1016/j.bbr.2009.07.020
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
010107 [宗教学]; 030301 [社会学]; 070906 [古生物学及地层学(含古人类学)];
摘要
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 (C) 2009 Elsevier B.V. All rights reserved
引用
收藏
页码:414 / 420
页数:7
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