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首页> 外文期刊>Cellular Physiology and Biochemistry >Bone Marrow Mesenchymal Stem Cell Transplantation Increases GAP-43 Expression via ERK1/2 and PI3K/Akt Pathways in Intracerebral Hemorrhage
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Bone Marrow Mesenchymal Stem Cell Transplantation Increases GAP-43 Expression via ERK1/2 and PI3K/Akt Pathways in Intracerebral Hemorrhage

机译：骨髓间充质干细胞移植通过ERK1 / 2和PI3K / Akt途径在脑出血中增加GAP-43表达。

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>Background/Aims: Intracerebral hemorrhage (ICH) occurs in hypertensive patients and results in high rates of mortality and disability. This study determined whether bone marrow mesenchymal stem cell (BMSC) transplantation affects axonal regeneration and examined the underlying mechanisms after the administration of PD98059 (p-ERK1/2 inhibitor) or/ and LY294002 (PI3K inhibitor). The hypothesis that was intended to be tested was that BMSC transplantation regulates the expression of growth-associated protein-43 (GAP-43) via the ERK1/2 and PI3K/Akt signaling pathways. Methods: Seventy-five male rats (250-280 g) were subjected to intracerebral blood injection and then randomly received a vehicle, BMSCs, PD98059 or LY294002 treatment. Neurological deficits were evaluated prior to injury and at 1, 3 and 7 days post-injury. The expression of GAP-43, Akt, p-Akt, ERK1/2, and p-ERK1/2 proteins was measured by western blot analysis. Results: BMSC transplantation attenuated neurological deficits 3-7 days post-ICH. The expression of GAP-43 was increased 3 days following BMSC transplantation. However, this increase was inhibited by either PD98059 or LY294002 treatment. Treatment with both PD98059 and LY294002 was more effective than was treatment with an individual compound. Conclusion: BMSC transplantation could attenuate neurological deficits and activate axonal regeneration in this rat ICH model. The protective effects might be associated with increased GAP-43 expression by activating both the ERK1/2 and PI3K/Akt signaling pathways.
机译：> 背景/目标： 高血压患者发生脑出血（ICH），导致高死亡率和致残率。这项研究确定了骨髓间充质干细胞（BMSC）移植是否影响轴突再生，并研究了PD98059（p-ERK1 / 2抑制剂）或/和LY294002（PI3K抑制剂）给药后的潜在机制。旨在测试的假设是BMSC移植通过ERK1 / 2和PI3K / Akt信号通路调节生长相关蛋白43（GAP-43）的表达。 方法： 对75只雄性大鼠（250-280 g）进行脑内注射，然后随机接受媒介物，BMSCs，PD98059或LY294002治疗。在损伤前以及损伤后1、3和7天评估神经功能缺损。通过蛋白质印迹分析测量GAP-43，Akt，p-Akt，ERK1 / 2和p-ERK1 / 2蛋白的表达。 结果： BMSC移植可减轻ICH后3-7天的神经功能缺损。 BMSC移植后3天，GAP-43的表达增加。但是，PD98059或LY294002处理均抑制了这种增加。用PD98059和LY294002进行的治疗均比使用单个化合物进行的治疗更为有效。 结论： 在该大鼠ICH模型中，BMSC移植可减轻神经功能缺损并激活轴突再生。通过激活ERK1 / 2和PI3K / Akt信号通路，保护作用可能与GAP-43表达增加有关。

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