Galectins are a group of β-galactoside-binding lectins associated with regulating immunological response. In the brains of AD patients and 5xFAD (familial AD) mice, galectin-3 (Gal-3) was highly upregulated and found to be expressed in microglia associated with Aβ plaques. However, the participation of other galectins, specifically galectin-9 (Gal-9) and T-cell immunoglobulin and mucin domain 3 (Tim-3) receptors, are unknown in the inflammatory response. The experimental model of the Aβ peptide will allow us to study the mechanisms of neuroinflammation and describe the changes in the expression of the Gal-9 and Tim-3 receptor. This study aimed to evaluate whether Aβ peptide administration into the lateral ventricles of rats upregulated Gal-9 and Tim-3 implicated in the modulation of neuroinflammation. The vehicle or Aβ peptide (1 μg/μL) was bilaterally administered into the of the rat, and control group. After the administration of the Aβ peptide, animals were tested for learning (day 29) and spatial memory (day 30) in the novel object recognition test (NOR). On day 31, hippocampus was examined for morphological changes by Nilss stain, biochemical changes by NO and MDA, immunohistochemical analysis by astrocytes (GFAP), microglia (Iba1), Gal-9 and Tim-3, and western blot. Our results show the administration of the Aβ peptide into the of rats induce memory impairment in the NOR by increases the oxidative stress and inflammatory response. This result is associated with an upregulation of Gal-9 and Tim-3 predominantly detected in the microglia cells of Aβ-treated rats with respect to the control group. Gal-9 and Tim-3 are upregulated in activated microglia that could modulate the inflammatory response and damage in neurodegenerative processes induced by the Aβ peptide. Therefore, we suggest that Gal-9 and Tim-3 participate in the inflammatory process induced by the administration of the Aβ peptide.

中文翻译：

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Galectin-9 和 Tim-3 因肽 Amyloid-β 诱导的小胶质细胞激活而上调 (25–35)

半乳糖凝集素是一组与调节免疫反应相关的β-半乳糖苷结合凝集素。在 AD 患者和 5xFAD（家族性 AD）小鼠的大脑中，半乳糖凝集素 3 (Gal-3) 高度上调，并被发现在与 Aβ 斑块相关的小胶质细胞中表达。然而，其他半乳糖凝集素，特别是半乳糖凝集素 9 (Gal-9) 和 T 细胞免疫球蛋白和粘蛋白结构域 3 (Tim-3) 受体在炎症反应中的参与尚不清楚。 Aβ肽的实验模型将使我们能够研究神经炎症的机制并描述Gal-9和Tim-3受体表达的变化。本研究旨在评估向大鼠侧脑室施用 Aβ 肽是否上调 Gal-9 和 Tim-3 与神经炎症调节有关。将媒介物或Aβ肽(1μg/μL)给予大鼠和对照组的双侧。施用 Aβ 肽后，在新物体识别测试 (NOR) 中测试动物的学习能力（第 29 天）和空间记忆能力（第 30 天）。第31天，通过尼尔斯染色检查海马的形态变化，通过NO和MDA进行生化变化，通过星形胶质细胞（GFAP）、小胶质细胞（Iba1）、Gal-9和Tim-3进行免疫组织化学分析，以及蛋白质印迹检查。我们的结果表明，将 Aβ 肽注射到大鼠脑中会通过增加氧化应激和炎症反应来诱导 NOR 记忆损伤。这一结果与 Gal-9 和 Tim-3 的上调有关，主要在 Aβ 治疗大鼠的小胶质细胞中检测到（相对于对照组）。 Gal-9 和 Tim-3 在激活的小胶质细胞中上调，可以调节 Aβ 肽诱导的神经退行性过程中的炎症反应和损伤。因此，我们认为 Gal-9 和 Tim-3 参与了 Aβ 肽诱导的炎症过程。