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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Toll-like receptor 2 promotes neurogenesis from the dentate gyrus after photothrombotic cerebral ischemia in mice
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Toll-like receptor 2 promotes neurogenesis from the dentate gyrus after photothrombotic cerebral ischemia in mice

机译：Toll样受体2促进小鼠光血栓性脑缺血后齿状回的神经发生

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The subgranular zone (SGZ) of hippocampal dentate gyrus (HDG) is a primary site of adult neurogenesis. Toll-like receptors (TLRs), are involved in neural system development of Drosophila and innate immune response of mammals. TLR2 is expressed abundantly in neurogenic niches such as adult mammalian hippocampus. It regulates adult hippocampal neurogenesis. However, the role of TLR2 in adult neurogenesis is not well studied in global or focal cerebral ischemia. Therefore, this study aimed to investigate the role of TLR2 in adult neurogenesis after photochemically induced cerebral ischemia. At 7 days after photothrombotic ischemic injury, the number of bromodeoxyuridine (BrdU)-positive cells was increased in both TLR2 knock-out (KO) mice and wild-type (WT) mice. However, the increment rate of BrdU-positive cells was lower in TLR2 KO mice compared to that in WT mice. The number of doublecortin (DCX) and neuronal nuclei (NeuN)-positive cells in HDG was decreased after photothrombotic ischemia in TLR2 KO mice compared to that in WT mice. The survival rate of cells in HDG was decreased in TLR2 KO mice compared to that in WT mice. In contrast, the number of cleaved-caspase 3 (apoptotic marker) and the number of GFAP (glia marker)/BrdU double-positive cells in TLR2 KO mice were higher than that in WT mice. These results suggest that TLR2 can promote adult neurogenesis from neural stem cell of hippocampal dentate gyrus through increasing proliferation, differentiation, and survival from neural stem cells after ischemic injury of the brain.
机译：海马齿状回（HDG）的亚颗粒区（SGZ）是成人神经发生的主要部位。 Toll样受体（TLR）参与果蝇的神经系统发育和哺乳动物的先天免疫应答。 TLR2在成年哺乳动物海马等神经源利基中大量表达。它调节成年海马神经发生。但是，TLR2在成人神经发生中的作用尚未在全脑或局灶性脑缺血中很好地研究。因此，本研究旨在研究TLR2在光化学诱导的脑缺血后在成人神经发生中的作用。在光血栓形成性缺血损伤后第7天，TLR2基因敲除（KO）小鼠和野生型（WT）小鼠中溴脱氧尿苷（BrdU）阳性细胞的数量均增加。然而，与WT小鼠相比，TLR2 KO小鼠中BrdU阳性细胞的增加率较低。与野生型小鼠相比，TLR2 KO小鼠发生光血栓性缺血后，HDG中双皮质素（DCX）和神经元核（NeuN）阳性细胞数量减少。与WT小鼠相比，TLR2 KO小鼠的HDG细胞存活率降低。相比之下，TLR2 KO小鼠中裂解的半胱天冬酶3（凋亡标记）和GFAP（神经胶质标记）/ BrdU双阳性细胞的数量高于野生型小鼠。这些结果表明TLR2可以通过增加脑缺血损伤后神经干细胞的增殖，分化和存活来促进海马齿状回神经干细胞的成年神经发生。

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