Assesment the role of oxidative stress and efficacy of caffeic acid phenethyl ester (CAPE) on neurotoxicity induced by isoniazid and ethambutol in a rat model.

OBJECTIVE The aim of this study were to investigate a role of oxidative stress and the therapeutic efficacy of caffeic acid phenethyl ester (CAPE) in the pathogenesis of neurotoxicity induced by isoniazid and etambutol in a rat model. MATERIALS AND METHODS Male Sprague-Dawley rats were randomly divided into eight experimental groups: control, INH, ETM, INH+ETM, INH+CAPE, ETM+CAPE, INH+ETM+CAPE, and CAPE treatment group, with ten animals in each group. INH and ETM doses were given orally within tap water for 30 days. CAPE was administered into relevant groups intraperitoneally for 30 days. Brain tissue and sciatic nerve were removed for biochemical and histopathological investigation. RESULTS In the INH, ETM, and INH+ETM groups, malondialdehyde (MDA) and total oxidant status (TOS) levels were significantly higher than those of the control group (p < 0.05). Also, in these groups, brain total antioxidant capacity (TAC) levels, and superoxide dismutase (SOD) and PON-1 activities were decreased compared with the control group (p < 0.05). By a CAPE supplement within INH and ETM groups, there was a significant decrease in MDA and TOS (p < 0.05). In addition to a significant increase in TAC levels, and SOD and PON-1 activities both in brain and sciatic nerve tissues (p < 0.05). CONCLUSIONS CAPE may protect against INH- and ETM-induced neurotoxicity in rat brain and sciatic nerve.