Toll-Like Receptor 2 Attenuates Traumatic Brain Injury-Induced Neural Stem Cell Proliferation in Dentate Gyrus of Rats
Toll-Like Receptor 2 Attenuates Traumatic Brain Injury-Induced Neural Stem Cell Proliferation in Dentate Gyrus of Rats
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DOI：
10.1155/2020/9814978
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发表时间：
2020-08-17
影响因子：
3.1
通讯作者：
He，Xiaosheng
中科院分区：
文献类型：
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作者：
Zhang，Xin;Hei，Yue;He，Xiaosheng
目前尚不清楚创伤性脑损伤（TBI）后炎症环境中神经干细胞（NSCs）如何以及是否对toll样受体2 （TLR2）作出反应。本研究利用大鼠脑外伤模型研究了TLR2与齿状回（DG） NSC增殖的相关性。采用免疫荧光法（IF）从形态学上观察BrdU、nestin、TLR2在DG中的表达。用胸腺嘧啶类似物5 -溴- 2 -脱氧尿苷（BrdU）标记DG中的增殖细胞。使用三标记BrdU、nestin和DAPI来鉴定新生成的NSCs。采用Western blotting和实时聚合酶链反应（real - time polymerase chain reaction， PCR）从蛋白和mRNA水平观察TLR2的表达。BrdU+细胞中BrdU+/nestin+/DAPI+细胞占84.30%±6.54%；DG中的BrdU+和nestin+细胞也是TLR2+细胞。BrdU+细胞和TLR2的表达（包括蛋白和mRNA水平）均在创伤后6小时(h)、24小时、3天(d)和7天立即升高，并在第3天达到峰值。结果表明，TLR2在DG（可能是NSCs）的增殖细胞上表达，TBI后TLR2的升高与NSCs的增殖存在潜在的相关性。综上所述，这些发现表明TLR2参与了脑外伤后DG的内源性神经发生。
It was not clear how and whether neural stem cells (NSCs) responded to toll‐like receptor 2 (TLR2) in the inflammatory environment after traumatic brain injury (TBI). The current study investigated the correlation of TLR2 and NSC proliferation in the dentate gyrus (DG) using the TBI model of rats. Immunofluorescence (IF) was used to observe the expression of BrdU, nestin, and TLR2 in the DG in morphology. Proliferating cells in the DG were labelled by thymidine analog 5‐bromo‐2‐deoxyuridine (BrdU). Three‐labelled BrdU, nestin, and DAPI was used for the identification of newly generated NSCs. Western blotting and real‐time polymerase chain reaction (PCR) were used to observe the expression of TLR2 from the level of protein and mRNA. We observed that BrdU+/nestin+/DAPI+cells accounted for 84.30%± 6.54%among BrdU+cells; BrdU+and nestin+cells in the DG were also TLR2+cells. BrdU+cells and the expression of TLR2 (both protein and mRNA levels) both elevated immediately at 6 hours (h), 24 h, 3 days (d), and 7 d posttrauma and peaked in 3 d. Results indicated that TLR2 was expressed on proliferating cells in the DG (NSCs possibly) and there was a potential correlation between increased TLR2 and proliferated NSCs after TBI. Taken together, these findings suggested that TLR2 was involved in endogenous neurogenesis in the DG after TBI.