We aimed to prove that oxidative stress is the main mechanism responsible for hippocampal neurotoxicity induced by deltamethrin (DLM). The protective role of curcumin (CMN) and nano-curcumin (NCMN) over this toxicity was studied. The rats were categorized into four groups: control, DLM, CMN and NCMN. The study continued for 30 days. Hippocampus was processed for histological, biochemical and immunohistochemical studies. Caspase-3, glial fibrillar acidic protein (GFAP), acetylcholinesterase (AChE), malondialdehyde (MDA), glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) were measured for DLM-induced oxidative stress (increased MDA by 354%/decreased GSH by 61%, SOD by 61%, CAT 57%). Oxidative stress induced apoptosis of hippocampal neurons through increasing Nrf2, gamma-glutamyl cysteine synthetase heavy subunit (GCS-HS) and light subunit (GCS-LS) and decreasing AChE. It increases the activity of astrocytes through increasing GFAP. Finally, oxidative stress has a bad impaction on cognitive function. Improvement of oxidative stress was observed with use of CMN and NCMN (decrease of MDA/increase of GSH, SOD, CAT). The level of Nrf2, GCS-HS and GCS-LS decreased, while AChE, GFAP increased. Improvement of cognitive function was observed in both groups. In conclusion, oxidative stress is the common mechanism responsible for DLM-induced hippocampal neurotoxicity. It exerts apoptosis of hippocampal neurons through increasing Nrf2, HS-GCS, LS-GCS and decreasing AChE. In addition, it activates astrocytes through increasing expression of GFAP. The protective role of CMN and CMMN is related to their potent antioxidant effect. Much improvement has been detected with NCMN as compared to CMN.

我们旨在证明氧化应激是溴氰菊酯（DLM）诱导海马神经毒性的主要机制。研究了姜黄素（CMN）和纳米姜黄素（NCMN）对这种毒性的保护作用。将大鼠分为四组：对照组，DLM，CMN和NCMN。研究持续了30天。对海马进行了组织学，生化和免疫组化研究。测量了Caspase-3，神经胶质原纤维酸性蛋白（GFAP），乙酰胆碱酯酶（AChE），丙二醛（MDA），谷胱甘肽（GSH），过氧化氢酶（CAT）和超氧化物歧化酶（SOD）的DLM诱导的氧化应激（MDA增加354） ％/ GSH降低61％，SOD降低61％，CAT降低57％）。氧化应激通过增加Nrf2诱导海马神经元凋亡，γ-谷氨酰半胱氨酸合成酶重亚基（GCS-HS）和轻亚基（GCS-LS）和AChE降低。它通过增加GFAP来增加星形胶质细胞的活性。最后，氧化应激对认知功能有不良影响。使用CMN和NCMN可以观察到氧化应激的改善（MDA降低/ GSH，SOD，CAT升高）。Nrf2，GCS-HS和GCS-LS的水平下降，而AChE，GFAP的水平上升。两组均观察到认知功能改善。总之，氧化应激是造成DLM诱导的海马神经毒性的常见机制。它通过增加Nrf2，HS-GCS，LS-GCS和降低AChE发挥海马神经元凋亡的作用。此外，它通过增加GFAP的表达来激活星形胶质细胞。CMN和CMMN的保护作用与其有效的抗氧化作用有关。与CMN相比，使用NCMN已检测到许多改进。