Investigation of the effects of vanilloids in chronic fatigue syndrome

• The chronic fatigue syndrome was produced using forced swim model for 21 days.
• Vanilloid receptor modulators (Agonist & Antagonist) were used to prevent/improve symptoms of chronic fatigue syndrome.
• Blocking of vanilloid receptors was found to be one of reason to improve symptoms.
• The agonist capsaicin showed partial antagonism and showed effects same as antagonist due to desensitization of receptors.

Aim of the studyTo assess the effectiveness of TRPV1 modulators in animal model of Chronic fatigue syndrome (CFS). To assess central and peripheral behavioral activity of TRPV1 modulators.Material and methodsCFS was induced by forcing the rats to swim for 10 min for 21 consecutive days. The rats were treated with capsaicin (TRPV1 agonist, 2.5 mg/kg) and n-tert-butylcyclohexanol (TRPV1 antagonist, 10 mg/kg) for 21 days 30 min before the exposure to stress procedure. The behavioral consequence of CFS was measured in terms of immobility time, grip strength, locomotor activity, and anxiety level using Rota rod, Actophotometer, and Elevated plus maze model respectively. The other parameters include Plasma corticosterone, adrenal gland and spleen weight, complete blood count, blood urea niterogen (BUN), Lactate dehydrogenase (LDH), Lipid peroxidation, catalase and reduced glutathione (GSH).Results and discussionTRPV1 modulators reversed (p < 0.05) the increase in immobility period, anxiety, spleen weight, BUN and LDH levels, and MDA levels along with decrease in grip strength, locomotor activity, plasma corticosterone, adrenal gland weight, catalase, and GSH. There was also significant increase in total WBC count when compared with the disease control group. The reversal was attributed to modulation of HPA axis, oxidative stress, anaerobic respiration product, muscle degradation product.ConclusionThe present study reveals the effectiveness of n-tert-butylcyclohexanol and capsaicin against chronic fatigue syndrome. The mechanism of action can be attributed to inhibition of TRPV1 channel and thereby modulating pain perception, neuroendocrine function, oxidative stress and immune function.