pharmacological and molecular evidence of neuroprotective curcumin effects against biochemical and behavioral sequels caused by methamphetamine: possible function of creb-bdnf signaling pathway

Introduction: the neuroprotective impact of curcumin and the role of creb (cyclic amp response element binding protein)-bdnf (brain-derived neurotrophic factor) signaling pathway was evaluated in methamphetamine (meth)-induced neurodegeneration in rats. methods: sixty adult male rats were randomly divided into 6 groups. while normal saline and 10 mg/kg meth were administered intraperitoneally in groups 1 and 2, groups 3, 4, 5, and 6 received meth (10 mg/kg) and curcumin (10, 20, 40, and 80 mg/kg, respectively) simultaneously. morris water maze test was administered, and oxidative hippocampal, antioxidant, inflammatory, apoptotic, and creb and bdnf were assessed. results: we found that meth disturbs learning and memory. concurrent curcumin therapy (40 and 80 mg/kg) decreased cognitive disturbance caused by meth. multiple parameters, such as lipid peroxidation, the oxidized form of glutathione, interleukin 1 beta, tumor necrosis factor-alpha, and bax were increased by meth therapy, while the reduced type of glutathione, bcl-2, p-creb, and bdnf concentrations in the hippocampus were decreased. conclusion: different doses of curcumin adversely attenuated meth-induced apoptosis, oxidative stress, and inflammation but enhanced the concentrations of p-creb and bdnf. the neuroprotection caused by curcumin against meth-induced neurodegeneration is mediated through p-creb-bdnf signaling pathway activation.