Department of Anatomy, College of Korean Medicine, Dongguk University, Gyeongju 38066, Republic of Korea.
Department of Food Science and Nutrition, Hallym University, Chuncheon 24252, Republic of Korea.
Int J Mol Sci. 2024 Mar 19;25(6):3461. doi: 10.3390/ijms25063461.
Aucubin, an iridoid glycoside, possesses beneficial bioactivities in many diseases, but little is known about its neuroprotective effects and mechanisms in brain ischemia and reperfusion (IR) injury. This study evaluated whether aucubin exhibited neuroprotective effects against IR injury in the hippocampal CA1 region through anti-inflammatory activity in gerbils. Aucubin (10 mg/kg) was administered intraperitoneally once a day for one week prior to IR. Neuroprotective effects of aucubin were assessed by neuronal nuclei (NeuN) immunofluorescence and Floro-Jade C (FJC) histofluorescence. Microgliosis and astrogliosis were evaluated using immunohistochemistry with anti-ionized calcium binding adapter protein 1 (Iba1) and glial fibrillary acidic protein (GFAP). Protein levels of proinflammatory cytokines interleukin1 beta (IL1β) and tumor necrosis factor alpha (TNFα) were assayed using enzyme-linked immunosorbent assay and Western blot. Changes in toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway were assessed by measuring levels of TLR4, inhibitor of NF-κB alpha (IκBα), and NF-κB p65 using Western blot. Aucubin treatment protected pyramidal neurons from IR injury. IR-induced microgliosis and astrogliosis were suppressed by aucubin treatment. IR-induced increases in IL1β and TNFα levels were significantly alleviated by the treatment. IR-induced upregulation of TLR4 and downregulation of IκBα were significantly prevented by aucubin treatment, and IR-induced nuclear translocation of NF-κB was reversed by aucubin treatment. Briefly, aucubin exhibited neuroprotective effects against brain IR injury, which might be related to the attenuation of neuroinflammation through inhibiting the TLR-4/NF-κB signaling pathway. These results suggest that aucubin pretreatment may be a potential approach for the protection of brain IR injury.
桃叶珊瑚苷，一种裂环环烯醚萜苷，具有许多疾病的有益生物活性，但对其在脑缺血再灌注（IR）损伤中的神经保护作用和机制知之甚少。本研究评估了桃叶珊瑚苷是否通过在沙土鼠中发挥抗炎活性对海马 CA1 区的 IR 损伤表现出神经保护作用。在 IR 前一周，每天通过腹腔内注射给予桃叶珊瑚苷（10mg/kg）一次。通过神经元核（NeuN）免疫荧光和 Floro-Jade C（FJC）组织荧光评估桃叶珊瑚苷的神经保护作用。通过用抗离子钙结合接头蛋白 1（Iba1）和胶质纤维酸性蛋白（GFAP）的免疫组织化学评估小胶质细胞和星形胶质细胞增生。通过酶联免疫吸附试验和 Western blot 测定促炎细胞因子白细胞介素 1β（IL1β）和肿瘤坏死因子α（TNFα）的蛋白水平。通过测量 TLR4/核因子-κB（NF-κB）信号通路中的 toll 样受体 4（TLR4）、NF-κB 抑制物α（IκBα）和 NF-κB p65 的水平来评估 TLR4/NF-κB 信号通路的变化。桃叶珊瑚苷治疗可保护锥体神经元免受 IR 损伤。桃叶珊瑚苷治疗可抑制 IR 诱导的小胶质细胞和星形胶质细胞增生。桃叶珊瑚苷治疗可显著减轻 IR 诱导的 IL1β 和 TNFα 水平升高。桃叶珊瑚苷治疗可显著防止 IR 诱导的 TLR4 上调和 IκBα 下调，并可逆转 IR 诱导的 NF-κB 核转位。简而言之，桃叶珊瑚苷对脑 IR 损伤表现出神经保护作用，这可能与通过抑制 TLR-4/NF-κB 信号通路减轻神经炎症有关。这些结果表明，桃叶珊瑚苷预处理可能是保护脑 IR 损伤的一种潜在方法。
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