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Amelioration of functional, biochemical and molecular deficits by epigallocatechin gallate in experimental model of alcoholic neuropathy.
Eur J Pain. 2011 Mar; 15(3):286-92.EJ

Abstract

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.

Authors+Show Affiliations

Pharmacology Research Laboratory, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh 160 014, India.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20699198

Citation

Tiwari, Vinod, et al. "Amelioration of Functional, Biochemical and Molecular Deficits By Epigallocatechin Gallate in Experimental Model of Alcoholic Neuropathy." European Journal of Pain (London, England), vol. 15, no. 3, 2011, pp. 286-92.
Tiwari V, Kuhad A, Chopra K. Amelioration of functional, biochemical and molecular deficits by epigallocatechin gallate in experimental model of alcoholic neuropathy. Eur J Pain. 2011;15(3):286-92.
Tiwari, V., Kuhad, A., & Chopra, K. (2011). Amelioration of functional, biochemical and molecular deficits by epigallocatechin gallate in experimental model of alcoholic neuropathy. European Journal of Pain (London, England), 15(3), 286-92. https://doi.org/10.1016/j.ejpain.2010.07.005
Tiwari V, Kuhad A, Chopra K. Amelioration of Functional, Biochemical and Molecular Deficits By Epigallocatechin Gallate in Experimental Model of Alcoholic Neuropathy. Eur J Pain. 2011;15(3):286-92. PubMed PMID: 20699198.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Amelioration of functional, biochemical and molecular deficits by epigallocatechin gallate in experimental model of alcoholic neuropathy. AU - Tiwari,Vinod, AU - Kuhad,Anurag, AU - Chopra,Kanwaljit, Y1 - 2010/08/10/ PY - 2010/03/18/received PY - 2010/07/01/revised PY - 2010/07/14/accepted PY - 2010/8/12/entrez PY - 2010/8/12/pubmed PY - 2011/8/24/medline SP - 286 EP - 92 JF - European journal of pain (London, England) JO - Eur J Pain VL - 15 IS - 3 N2 - 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. SN - 1532-2149 UR - https://www.unboundmedicine.com/medline/citation/20699198/Amelioration_of_functional_biochemical_and_molecular_deficits_by_epigallocatechin_gallate_in_experimental_model_of_alcoholic_neuropathy_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1090-3801(10)00171-0 DB - PRIME DP - Unbound Medicine ER -