Protective Effect of Epigallocatechin Gallate in Murine Water‐Immersion Stress Model of Chronic Fatigue Syndrome

Abstract

Chronic fatigue syndrome (CFS) is a specific clinical condition that characterizes unexplained disabling fatigue. In the present study, chronic fatigue was produced in mice by subjecting them to forced swim inside a rectangular jar of specific dimensions for 6 min. daily for 15 days. Epigallocatechin gallate (EGCG; 25, 50 and 100 mg ⁄ kg, p.o.) was administered daily 30 min. before forced swim session. Immobility period and post-swim fatigue was assessed on alternate days. On the 16th day, after assessment of various behavioural parameters, mice were killed to harvest the brain, spleen and thymus. There was significant increase in oxidative-nitrosative stress and tumour necrosis factor-a levels in the brain of mice subjected to water-immersion stress as compared with naive group. These behavioural and biochemical alterations were restored after chronic treatment with EGCG. The present study points out that EGCG could be of therapeutic potential in the treatment of chronic fatigue.

Antifatigue Effect of Luteolin‐6‐C‐Neohesperidoside on Oxidative Stress Injury Induced by Forced Swimming of Rats through Modulation of Nrf2/ARE Signaling Pathways

“…The doses of LN and ascorbic acid were decided based on our preliminary tests (data not shown) and previous studies [27]. LN and ascorbic acid were dissolved in distilled water and were orally administrated once daily for 3 weeks, 1 h before forced treadmill exercise.…”

Downregulation of tumor necrosis factor and other proinflammatory biomarkers by polyphenols

“…inhibited LPS-induced anorexia in rats [57]. EGCG Chronic treatment with EGCG significantly reduced TNF-a level and fatigue in mice [65].…”

“…At the molecular level, inflammation 53 is regulated by numerous molecules and factors, including cyto- 54 kines [interleukin (IL)-1, IL-2, IL-6, IL-12, tumor necrosis factor 55 (TNF)-a, TNF-b], 1 chemokines (monocyte chemoattractant protein 56 1, IL-8), proinflammatory transcription factors [nuclear factor- 57 kappaB (NF-jB), signal transducer and activator of transcription 58 (STAT)-3], proinflammatory enzymes [cyclooxygenase (COX)-2, 59 5-lipoxygenase (LOX), 12-LOX, matrix metalloproteinases (MMPs), 60 prostate-specific antigen (PSA), C-reactive protein, adhesion http 62 adhesion molecule (VCAM)-1, endothelial-leukocyte adhesion mole- 63 cule (ELAM)-1), vascular endothelial growth factor (VEGF), and 64 TWIST [1]. Among all these mediators, NF-jB is the central regulator 65 of inflammation [1,2]. It has been shown to activate more than 500 66 genes, most of which are implicated in inflammation [3,4].…”

Lycopene abrogates Aβ(1–42)-mediated neuroinflammatory cascade in an experimental model of Alzheimer’s disease

“…The time taken by the rat to enter the closed arm in the first trial (acquisition trial) on the 14th day was noted and was called the initial transfer latency. Cutoff time was fixed at 90 s, and in case a rat could not find the closed arm within this period, it was gently pushed into one of the closed arms and allowed to explore the maze for 30 s. The second trial (retention trial) was performed 24 h after the acquisition trial, and retention transfer latency was noted [28]. The retention trial latency was expressed as percentage of initial trial latency.…”