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首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >Curcumin pretreatment protects against hypoxia/reoxgenation injury via improvement of mitochondrial function, destabilization of HIF-1 alpha and activation of Epac1-Akt pathway in rat bone marrow mesenchymal stem cells
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Curcumin pretreatment protects against hypoxia/reoxgenation injury via improvement of mitochondrial function, destabilization of HIF-1 alpha and activation of Epac1-Akt pathway in rat bone marrow mesenchymal stem cells

机译：姜黄素预处理通过改善线粒体功能，HIF-1α的破坏化和大鼠骨髓间充质干细胞中的HIF-1α的稳定化和活化的活化的预处理来保护缺氧/雷诺治疗。

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Bone marrow mesenchymal stem cells (BMSCs) possess promising therapeutic effects and have been considered as a highly desirable agent for tissue injury treatment. However, little survived cells after transplanting due to severe relocated conditions (characterized by prolonged hypoxia and oxidative stress) lead to hampered benefits of BMSCs-based cell therapy. Curcumin, a natural dietary product, has attracted increasing attention owing to its profound pharmacologic properties. Here, we report the protective effects of curcumin pretreatment in BMSCs against hypoxia and reoxygenation (H/R) triggered injury, which mimick ischemia/reperfusion in vivo. We found that curcumin pretreatment remarkably inhibited H/R-induced cell viability loss, cell nuclei condensation, LDH leakage, as well as caspase-3 activity increase in BMSCs. Furthermore, curcumin pretreatment prevented H/R-induced mitochondrial dysfunction through expediting adenosine triphosphate production and suppressing reactive oxygen species accumulation and mitochondrial membrane potential decline. In addition, curcumin pretreatment notably induced HIF-1 alpha destabilization, Epac1 and Akt activation, and Erk1/2 and p38 deactivation. However, Epacl inhibitor ESI-09 obviously restrained the increase of p-Akt induced by curcumin, but not p-Erk1/2 or p-p38, and abrogated the protective effect of curcumin on BMSCs' survival and arrested cell cycle in G0/G1 phase. Taken together, these results demonstrated that curcumin pretreatment conferred BMSCs the ability to survive from H/R injury, which might attribute to its protection on mitochondrial function, destabilization of HIF-1 alpha and activation of Epac1-Akt signaling pathway. Thus, this study provides more pharmacologic aspects of curcumin, and suggests that pre-conditioning of BMSCs with curcumin could serve as an attractive approach for facilitating cell therapy in tissue repair treatment.
机译：骨髓间充质干细胞（BMSC）具有有前途的治疗效果，并且被认为是用于组织损伤治疗的非常理想的药剂。然而，由于严重的重接条件（以延长的缺氧和氧化应激为特征）导致BMSC的细胞疗法的受益效果，移植后移植后少于存活的细胞。由于其深厚的药理学性质，姜黄素是一种天然膳食产品，引起了越来越关注的药理学。在这里，我们报告了姜黄素预处理在BMSCs抗缺氧和雷诺酸（H / R）触发损伤中的保护作用，其在体内模仿缺血/再灌注。我们发现姜黄素预处理显着抑制H / R诱导的细胞活力损失，细胞核缩合，LDH泄漏，以及BMSCs的Caspase-3活性增加。此外，姜黄素预处理通过加速三磷酸三磷酸盐产生并抑制反应性氧物种积累和线粒体膜势下降，防止了H / R诱导的线粒体功能障碍。此外，姜黄素预处理显着诱导HIF-1α稳定，EPAC1和AKT激活，ERK1 / 2和P38去激活。然而，Epacl抑制剂ESI-09明显抑制了姜黄素诱导的p-akt的增加，但不是P-ERK1 / 2或P-P38，并且废除了G0 / G1中BMSC的生存和被捕细胞周期的保护作用阶段。这些结果表明，姜黄素预处理赋予BMSCS从H / R损伤中存活的能力，这可能归因于其对线粒体功能的保护，HIF-1α的稳定化和EPAC1-AKT信号通路的激活。因此，该研究提供了姜黄素的更多药理学方面，并提出了具有姜黄素的BMSCs的预调节可以作为促进组织修复处理中细胞疗法的吸引力的方法。

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