Protective efficacy of curcumin in arsenic induced NMDA receptor dysfunctions and PI3K/Akt/ GSK3β signalling in hippocampus has been investigated in vivo and in vitro. Exposure to sodium arsenite (in vivo – 20 mg/kg, body weight p.o. for 28 days; in vitro – 10 μM for 24 h) and curcumin (in vivo – 100 mg/kg body weight p.o. for 28 days; in vitro – 20 μM for 24 h) was carried out alone or simultaneously. Treatment with curcumin ameliorated sodium arsenite induced alterations in the levels of NMDA receptors, its receptor subunits and synaptic proteins - pCaMKIIα, PSD-95 and SynGAP both in vivo and in vitro. Decreased levels of BDNF, pAkt, pERK1/2, pGSK3β and pCREB on sodium arsenite exposure were also protected by curcumin. Curcumin was found to decrease sodium arsenite induced changes in hippocampus by modulating PI3K/Akt/GSK3β neuronal survival pathway, known to regulate various cellular events. Treatment of hippocampal cultures with pharmacological inhibitors for ERK1/2, GSK3β and Akt individually inhibited levels of CREB and proteins associated with PI3K/Akt/GSK3β pathway. Simultaneous treatment with curcumin was found to improve sodium arsenite induced learning and memory deficits in rats assessed by water maze and Y-maze. The results provide evidence that curcumin exercises its neuroprotective effect involving PI3K/Akt pathway which may affect NMDA receptors and downstream signalling through TrKβ and BDNF in arsenic induced cognitive deficits in hippocampus.

姜黄素对砷诱导的海马中NMDA受体功能障碍和PI3K / Akt /GSK3β信号转导的保护作用已在体内和体外进行了研究。暴露于亚砷酸钠（体内– 20 mg / kg，体重，口服28天；体外– 10μM，24小时）和姜黄素（体内– 100 mg / kg体重，口服28天；体外– 20天单独或同时进行24小时（μM）。用姜黄素改善的亚砷酸钠治疗在体内和体外均可引起NMDA受体，其受体亚基和突触蛋白-pCaMKIIα，PSD-95和SynGAP的水平改变。姜黄素还可以保护暴露于亚砷酸钠的BDNF，pAkt，pERK1 / 2，pGSK3β和pCREB水平降低。发现姜黄素可通过调节PI3K / Akt /GSK3β神经元存活途径（可调节各种细胞事件）来减少亚砷酸钠诱导的海马体变化。用ERK1 / 2，GSK3β和Akt的药理抑制剂治疗海马培养物可分别抑制CREB和PI3K / Akt /GSK3β途径相关蛋白的水平。发现用姜黄素同时治疗可改善由水迷宫和Y迷宫评估的大鼠亚砷酸钠诱导的学习和记忆障碍。结果提供了证据，姜黄素在涉及砷引起的海马认知障碍中，可能通过PI3K / Akt途径行使其神经保护作用，而PI3K / Akt途径可能会影响NMDA受体以及通过TrKβ和BDNF的下游信号传导。用ERK1 / 2，GSK3β和Akt的药理抑制剂治疗海马培养物可分别抑制CREB和PI3K / Akt /GSK3β途径相关蛋白的水平。发现用姜黄素同时治疗可改善由水迷宫和Y迷宫评估的大鼠亚砷酸钠诱导的学习和记忆障碍。结果提供了证据，姜黄素在涉及砷引起的海马认知障碍中，可能通过PI3K / Akt途径行使其神经保护作用，而PI3K / Akt途径可能会影响NMDA受体以及通过TrKβ和BDNF的下游信号传导。用ERK1 / 2，GSK3β和Akt的药理抑制剂治疗海马培养物可分别抑制CREB和PI3K / Akt /GSK3β途径相关蛋白的水平。发现用姜黄素同时治疗可改善由水迷宫和Y迷宫评估的大鼠亚砷酸钠诱导的学习和记忆障碍。结果提供了证据，姜黄素在涉及砷引起的海马认知障碍中，可能通过PI3K / Akt途径行使其神经保护作用，而PI3K / Akt途径可能会影响NMDA受体以及通过TrKβ和BDNF的下游信号传导。