ABSTRACT
Objective To investigate the efficacy of treatment and prevention of VitE on vacuous chewing move-ments (VCMs) of haloperidol-induced tardive dyskinesia (TD) rats and serum levels of brain-derived neurotrophic fac-tor ( BDNF) and total antioxidant capacity ( TAC) , and to explore the possible mechanisms.Methods Thirty-two male Sprague-Dawley (SD) rats were randomly divided into TD, P-Vit E, T-Vit E and control group (n=8), receiving to-week treatment with Haloperidol (Hal)+NS, Hal+Vit E (medicated at the baseline), Hal+VitE (medicated at the fifth week) or normal saline (NS), respectively.VCM was evaluated at each week.ELISA and spectrophotometer were used to detect the serum levels of BDNF and TAC, respectively.Results The VCM score of both TD group and T-Vit E group increased at the 2nd weekend, reached the peak at the 5th weekend.VCM score of T-Vit E group declined gradually at the 6th weekend and was significantly lower than that in the TD group [(6.5 ±3.3) vs.(27.9 ±5.8), P0.05) at the 10th weekend.There was no significant difference in VCM score between P-Vit E group and control group for ten weeks(P>0.05).At the 10th weekend, serum BDNF [(6.9 ±1.0) pg/mL] and TAC [(11.9 ±3.2) U/mL] levels of TD group were significantly lower than those of the controls [BDNF (8.6 ±2.5) pg/mL, TAC (18.2 ±5.5) U/mL] and T-Vit E group [BDNF (8.7 ±2.0) pg/mL, (18.6 ±5.9) U/mL] (P0.05).Conclusions Vit E may relieve and prevent VCM in TD model rats though alleviation of free radical damage.