Elucidation of molecular mechanism involved in neuroprotective effect of Coenzyme Q10 in alcohol-induced neuropathic pain

The aim of the present investigation was to evaluate the effect of Coenzyme Q10 and its combination with vitamin E in alcohol-induced chronic neuropathic pain. Male Wistar rats were orally treated with alcohol (10g/kg, 35% v/v, b.i.d.) for 10weeks. Coenzyme Q10 (25, 50, and 100mg/kg) and vitamin E (100mg/kg) were coadministered orally for 1h after ethanol administration for 10weeks. Various nerve functions, biochemical, and molecular parameters were assessed. Chronic administration of ethanol for 10weeks resulted significant development of neuropathic pain. Treatment with Coenzyme Q10 (50 and 100mg/kg) for 10weeks showed significant and dose dependently increased in level of nociceptive threshold, endogenous antioxidant, and Na,K-ATPase enzyme. Coenzyme Q10 (50 and 100mg/kg) significantly restored the levels of motor nerve conduction velocity and sensory nerve conduction velocity. It also showed significant decrease in levels of endogenous calcium, oxidative-nitrosative stress, TNF-, IL-1, and IL-4 level. Alteration in protein expression of polymerase gamma (pol ) was significantly restored the Coenzyme Q10 treatment. The important finding of the study is that, Coenzyme Q10 (100mg/kg) and -tocopherol (100mg/kg) combination-treated rats showed more significant prevention of behavioral, biochemical, and molecular neurotoxic effect of alcohol administration than Coenzyme Q10 or -tocopherol alone treated group. It is evident from the finding of present investigation that plethora of mechanism including inhibition of oxido-nitrosative stress, release of pro-inflammatory cytokine, modulation of endogenous biomarker, and protection of pol protein expression simultaneously orchestrate to exhibits neuroprotective effect of Coenzyme Q10, vitamin E and their combination.