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首页> 外文期刊>Biomolecules & therapeutics >Pretreatment with Lycopene Attenuates Oxidative Stress-Induced Apoptosis in Human Mesenchymal Stem Cells
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Pretreatment with Lycopene Attenuates Oxidative Stress-Induced Apoptosis in Human Mesenchymal Stem Cells

机译：番茄红素预处理可减轻人间充质干细胞中氧化应激诱导的细胞凋亡。

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Human mesenchymal stem cells (MSCs) have been used in cell-based therapy to promote revascularization after peripheral or myocardial ischemia. High levels of reactive oxygen species (ROS) are involved in the senescence and apoptosis of MSCs, causing defective neovascularization. Here, we examined the effect of the natural antioxidant lycopene on oxidative stress-induced apoptosis in MSCs. Although H2O2 (200 mu M) increased intracellular ROS levels in human MSCs, lycopene (10 mu M) pretreatment suppressed H2O2-induced ROS generation and increased survival. H2O2-induced ROS increased the levele of phosphorylated p38 mitogen activated protein kinase (MAPK), Jun-N-terminal kinase (JNK), ataxia telangiectasia mutated (ATM), and p53, which were inhibited by lycopene pretreatment. Furthermore, lycopene pretreatment decreased the expression of cleaved poly (ADP ribose) polymerase-1 (PARP-1) and caspase-3 and increased the expression of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax), which were induced by H2O2 treatment. Moreover, lycopene significantly increased manganese superoxide dismutase (MnSOD) expression and decreased cellular ROS levels via the PI3K-Akt pathway. Our findings show that lycopene pretreatment prevents ischemic injury by suppressing apoptosis-associated signal pathway and enhancing anti-oxidant protein, suggesting that lycopene could be developed as a beneficial broad-spectrum agent for the successful MSC transplantation, in ischemic diseases.
机译：人间充质干细胞（MSCs）已用于基于细胞的治疗，以促进周围或心肌缺血后的血运重建。高水平的活性氧（ROS）参与了MSC的衰老和凋亡，导致新血管形成不良。在这里，我们检查了天然抗氧化剂番茄红素对氧化应激诱导的细胞凋亡的影响。尽管H2O2（200μM）增加了人MSC中细胞内ROS的水平，但是番茄红素（10μM）预处理抑制了H2O2诱导的ROS的产生并提高了存活率。 H2O2诱导的ROS增加了番茄红素预处理抑制的磷酸化p38丝裂原活化蛋白激酶（MAPK），Jun-N-末端激酶（JNK），共济失调毛细血管扩张突变（ATM）和p53的水平。此外，番茄红素预处理可降低裂解的多聚（ADP核糖）聚合酶-1（PARP-1）和caspase-3的表达，并增加B细胞淋巴瘤2（Bcl-2）和与Bcl-2相关的X蛋白的表达（ Bax），这是由H2O2处理诱导的。此外，番茄红素通过PI3K-Akt途径显着增加了锰超氧化物歧化酶（MnSOD）的表达并降低了细胞ROS的水平。我们的发现表明，番茄红素预处理可通过抑制凋亡相关信号通路和增强抗氧化蛋白来预防缺血性损伤，这表明番茄红素可作为缺血性疾病成功进行MSC移植的有益广谱药物。

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