Bone marrow mesenchymal stem cell (BMSCs) -based therapies represent a promising treatment for neurological disorders. However, therapeutic effects and mechanisms of BMSCs transplantation for radiation-induced brain injury (RIBI) have not been fully disclosed. In this article, we explored the functions of BMSCs transplantation on RIBI and investigated the protective effects of BMSCS on hippocampal neurons in RIBI as well as the related molecular mechanisms. 6–8 weeks-old rats were used to build a RIBI model. Rats in BMSC group were treated with a 3 × 10 BMSCs injection through the tail vein on the 1st day and 8th day after irradiation; rats in both control and RIBI groups were injected with an equivalent volume of physiological saline for comparisons. The Morris water maze was applied to detect the variations in cognitive function after RIBI. MRS was performed to test changes in NAA/Cr, indicating neuronal apoptosis after RIBI. TUNEL was conducted to detect apoptosis of rat hippocampal neurons, and HE staining was carried out to show pathological variations in the hippocampal region of rats. Protein levels of PI3K, P-PI3K, AKT, P-AKT, Bcl-2, and Bax proteins of rats in the hippocampal area were all determined by Western blot. Cognitive function was reduced and hippocampal neurons underwent apoptosis in the rats of the RIBI group, and cognitive abilities, histopathological alterations, and apoptosis of hippocampal neurons were significantly improved after BMSCs treatment; the expression of PI3K, P-PI3K, AKT, P-AKT, and Bcl-2 proteins, in the hippocampal region of the rat, was up-regulated, and Bax proteins were down-regulated. BMCSs can inhibit hippocampal neuronal apoptosis in RIBI, and the mechanism may be associated with the up-regulation of Bcl-2 and down-regulation of Bax by the PI3K/AKT signaling pathway.

中文翻译：

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BMSCs 通过 PI3K/Akt/Bax/Bcl-2 信号通路减轻辐射引起的脑损伤诱导的海马神经元凋亡

基于骨髓间充质干细胞（BMSC）的疗法是治疗神经系统疾病的一种有前景的疗法。然而，骨髓间充质干细胞移植治疗放射性脑损伤（RIBI）的治疗效果和机制尚未完全公开。本文探讨BMSCs移植对RIBI的作用，探讨BMSCs对RIBI海马神经元的保护作用及相关分子机制。采用6-8周龄大鼠建立RIBI模型。 BMSC组大鼠于照射后第1天和第8天经尾静脉注射3×10个BMSCs；对照组和RIBI组大鼠均注射等量生理盐水进行比较。采用Morris水迷宫检测RIBI后认知功能的变化。 MRS 检测 NAA/Cr 的变化，表明 RIBI 后神经元凋亡。 TUNEL检测大鼠海马神经元凋亡，HE染色显示大鼠海马区病理变化。采用Western blot法测定大鼠海马区PI3K、P-PI3K、AKT、P-AKT、Bcl-2、Bax蛋白水平。 RIBI组大鼠认知功能下降、海马神经元凋亡，BMSCs治疗后认知能力、组织病理学改变和海马神经元凋亡均明显改善；大鼠海马区PI3K、P-PI3K、AKT、P-AKT、Bcl-2蛋白表达上调，Bax蛋白表达下调。 BMCSs可抑制RIBI中海马神经元凋亡，其机制可能与PI3K/AKT信号通路上调Bcl-2、下调Bax有关。