This study aims to explore the effect of Tectorigenin in chronic cerebral ischemia (CCI)-induced cognitive impairment mice model. Cognitive impairment, hippocampal tissue histopathology, and myelin density in CCI mice were detected. HT22 cells were used to induce oxygen-glucose deprivation/reperfusion (OGD/R) injury. Cell viability and apoptosis of transfected HT22 cells and toll-like receptor-4 (TLR4)/nuclear factor-kappaB (NF-κB) pathway-related factor levels in hippocampal tissue and OGD/R models were detected. CCI caused cognitive impairment, hippocampal damage, and decreased myelin density in mice while promoting interleukin-1β, tumor necrosis factor-alpha, TLR4, myeloid differentiation primary response gene 88, p-p65, NLRP3, and ASC levels. Tectorigenin reversed the effects of CCI in mice and reversed the promoting effects of OGD/R on apoptosis and TLR4/NF-κB pathway-related factors levels, while overexpressed TLR4 reversed the effects of Tectorigenin in OGD/R-induced HT-22 cells. Tectorigenin alleviated cognitive impairment in CCI mice by inhibiting the TLR4/NF-κB signaling pathway.

中文翻译：

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Tectorigenin 通过抑制 TLR4/NF-κB 信号通路减轻慢性脑缺血小鼠的认知障碍。

本研究旨在探讨Tectorigenin在慢性脑缺血（CCI）诱导的认知障碍小鼠模型中的作用。检测到 CCI 小鼠的认知障碍、海马组织病理学和髓鞘密度。HT22 细胞用于诱导氧-葡萄糖剥夺/再灌注 (OGD/R) 损伤。检测转染HT22细胞的细胞活力和凋亡情况，检测海马组织和OGD/R模型中toll样受体4（TLR4）/核因子-κB（NF-κB）通路相关因子水平。CCI 导致小鼠认知障碍、海马损伤和髓鞘密度降低，同时促进白细胞介素-1β、肿瘤坏死因子-α、TLR4、骨髓分化初级反应基因 88、p-p65、NLRP3 和 ASC 水平。Tectorigenin 在小鼠中逆转 CCI 的作用并逆转 OGD/R 对细胞凋亡和 TLR4/NF-κB 通路相关因子水平的促进作用，而过表达的 TLR4 逆转 TLR4 在 OGD/R 诱导的 HT-22 细胞中的作用。Tectorigenin 通过抑制 TLR4/NF-κB 信号通路减轻 CCI 小鼠的认知障碍。