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首页> 外文期刊>Biological chemistry >Changqin NO. 1 inhibits neuronal apoptosis via suppressing GAS5 expression in a traumatic brain injury mice model
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Changqin NO. 1 inhibits neuronal apoptosis via suppressing GAS5 expression in a traumatic brain injury mice model

机译：长查没有。 1通过抑制创伤性脑损伤小鼠模型中的抑制气体5表达来抑制神经元细胞凋亡

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The present study was designed to investigate the mechanism of the traditional Chinese medicine Changqin NO. 1 on the amelioration of traumatic brain injury (TBI). Adult male C57BL/6J mice and newborn mice were used to generate a mouse TBI model and harvest primary neurons, respectively. The localizations of specific neural markers neuropilin-1 (Nrp-1), growth-associated protein-43 (GAP-43) and microtubule-associated protein Tau (Tau) were examined in brain tissues by immunohistochemistry. Terminal deoxynucleotidyl transferase dUTP nick end labeling apoptotic cell detection in tissue sections and the CCK-8 cell viability assay were performed to examine neuronal apoptosis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were also carried out in this study. The association between long non-coding RNA (lncRNA) growth-arrest specific 5 (GAS5), miR-335 and RAS p21 GTPase activating protein 1 (Rasa1) was disclosed using the dual-luciferase reporter assay. Changqin NO. 1 inhibited TBI-induced neuronal apoptosis in vivo and in vitro. GAS5 functioned as a competing endogenous RNA (ceRNA) by sponging miR-335 to upregulate Rasa1 expression in mouse neuronal cells. Further investigations demonstrated that GAS5 promoted neuronal apoptosis following TBI via the miR-335/Rasa1 axis. In vivo experiments indicated that Changqin NO. 1 exerted neuroprotection during TBI via the GAS5/miR-335/Rasa1 axis. Changqin NO. 1 promoted neuroprotective effects by inhibiting neuronal apoptosis via the GAS5/miR-335/Rasa1 axis in TBI.
机译：本研究旨在调查中医药的机制长查未。 1关于创伤性脑损伤的改善（TBI）。成年男性C57BL / 6J小鼠和新生儿分别用于产生小鼠TBI模型和收获原发性神经元。通过免疫组织化学在脑组织中检查了特异性神经标记物神经标记物神经标记神经素-1（NRP-1），生长相关的蛋白-43（GAP-43）和微管相关蛋白质TAU（TAU）。末端脱氧核苷酸转移酶DUTP缺口末端标记组织切片中的凋亡细胞检测和CCK-8细胞活力测定以检查神经元细胞凋亡。本研究还进行了定量实时聚合酶链反应（QRT-PCR）和Western印迹。使用双荧光素酶报告分析，公开了长期非编码RNA（LNCRNA）生长捕获特异性5（GAS5），MIR-335和RAS P21 GTP酶活化蛋白1（RASA1）之间的关联。长查没有。 1抑制TBI诱导的体内和体外神经元细胞凋亡。气体5通过冲水MiR-335作为竞争内源RNA（Cerna）用作在小鼠神经元细胞中上调RASA1表达。进一步的研究表明，通过MIR-335 / RASA1轴线，Gas5促进了TBI之后的神经细胞凋亡。在体内实验中表明长查文没有。 1通过Gas5 / miR-335 / RASA1轴在TBI期间施加神经保护。长查没有。 1通过TBI中的Gas5 / miR-335 / RASA1轴抑制神经元细胞凋亡来促进神经保护作用。

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