Evaluation of ameliorative effect of quercetin in experimental model of alcoholic neuropathy in rats.

OBJECTIVE

The objective of the present investigation was to study the neuroprotective effect of the quercetin in alcohol induced neuropathy in rats.

MATERIALS AND METHODS

Male Wistar rats were administered alcohol (10 gm/kg, 35% v/v, p.o. b.i.d.) for 10 weeks. Alpha tocopherol (vitamin E) was used as a standard drug. Vitamin E (100 mg/kg) and quercetin (10, 20 and 40 mg/kg) were co-administered 1 h after ethanol administration for 10 weeks. Behavioral assessment parameters, such as motor incoordination, tactile allodynia, mechanical and thermal hyperalgesia were recorded in all groups of animals. Meanwhile, motor nerve conduction velocity was also recorded. Biochemical parameters, such as nitric oxide (NO), Na(+)-K(+)-ATPase, malondialdehyde (MDA) and myeloperoxidase (MPO) were estimated in sciatic nerve. Apoptosis index was determined with help of DNA fragmentation in sciatic nerve.

RESULTS AND DISCUSSION

Chronic ethanol administration for 10 weeks resulted in significant (P < 0.001) development of neuropathic pain. Chronic treatment with quercetin (20 and 40 mg/kg) for 10 weeks significantly (P < 0.001) attenuated allodynia, hyperalgesia as well as motor coordination and impaired nerve conduction velocity along with decreased level of membrane-bound Na(+)-K(+)-ATPase. It also significantly (P < 0.001) decreased elevated levels of MDA, MPO as well as pro-inflammatory mediators, such as NO. It also decreased the extent of DNA fragmentation. This alteration was more significant in vitamin E treated rats (100 mg/kg). Quercetin is a proven antioxidant that might have decreased the oxidative stress produced by chronic alcoholism.

CONCLUSION

The present investigation elucidates neuroprotective effect of quercetin in alcohol induced neuropathy through modulation of membrane-bound inorganic phosphate enzyme and inhibition of release of oxido-inflammatory mediators, such as MDA, MPO and NO.