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Amelioration of functional, biochemical and molecular deficits by epigallocatechin gallate in experimental model of alcoholic neuropathy
Author(s) -
Tiwari Vinod,
Kuhad Anurag,
Chopral Kanwaljit
Publication year - 2011
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1016/j.ejpain.2010.07.005
Subject(s) - hyperalgesia , neuropathic pain , allodynia , pharmacology , neuroprotection , oxidative stress , medicine , threshold of pain , capsaicin , nociception , anesthesia , chemistry , receptor
Long term alcohol consumption leads to decreased nociceptive threshold characterized by spontaneous burning pain, hyperalgesia and allodynia. The mechanism involved in this pain includes increased oxidative‐nitrosative stress, release of pro‐inflammatory cytokines and neuronal apoptosis. The present study was designed to explore the protective effect of epigallocatechin‐3‐gallate against alcoholic neuropathic pain in rats. Rats fed with alcohol (35%) for 10 weeks showed markedly decreased tail flick latency in tail‐immersion test (thermal hyperalgesia), vocalization threshold in Randall—Sellito test (mechanical hyperalgesia) and paw‐withdrawal threshold in von‐Frey hair test (mechanical allodynia) along with enhanced oxidative‐nitrosative stress and inflammatory mediators (TNF‐α, IL‐1β and TGF‐β1 levels). Co‐administration of epigallocatechin‐3‐gallate (25–100 mg/kg) significantly and dose‐dependently prevented functional, biochemical and molecular changes associated with alcoholic neuropathy. In conclusion, the current findings suggest the neuroprotective potential of epigallocatechin‐3‐gallate in attenuating the functional, biochemical and molecular alterations associated with alcoholic neuropathy through modulation of oxido‐inflammatory cascade.