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首页> 外文期刊>Cellular Physiology and Biochemistry >Pre-Treatment with Melatonin Enhances Therapeutic Efficacy of Cardiac Progenitor Cells for Myocardial Infarction
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Pre-Treatment with Melatonin Enhances Therapeutic Efficacy of Cardiac Progenitor Cells for Myocardial Infarction

机译：褪黑素预处理可增强心肌祖细胞治疗心肌梗塞的疗效

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Background/Aims Melatonin possesses many biological activities such as antioxidant and anti-aging. Cardiac progenitor cells (CPCs) have emerged as a promising therapeutic strategy for myocardial infarction (MI). However, the low survival of transplanted CPCs in infarcted myocardium limits the successful use in treating MI. In the present study, we aimed to investigate if melatonin protects against oxidative stress-induced CPCs damage and enhances its therapeutic efficacy for MI. Methods TUNEL assay and EdU assay were used to detect the effects of melatonin and miR-98 on H2O2-induced apoptosis and proliferation. MI model was used to evaluate the potential cardioprotective effects of melatonin and miR-98. Results Melatonin attenuated H2O2-induced the proliferation reduction and apoptosis of c-kit+ CPCs in vitro, and CPCs which pretreated with melatonin significantly improved the functions of post-infarct hearts compared with CPCs alone in vivo. Melatonin was capable to inhibit the increase of miR-98 level by H2O2 in CPCs. The proliferation reduction and apoptosis of CPCs induced by H2O2 was aggravated by miR-98. In vivo, transplantation of CPCs with miR-98 silencing caused the more significant improvement of cardiac functions in MI than CPCs. MiR-98 targets at the signal transducer and activator of the transcription 3 (STAT3), and thus aggravated H2O2-induced the reduction of Bcl-2 protein. Conclusions Pre-treatment with melatonin protects c-kit+ CPCs against oxidative stress-induced damage via downregulation of miR-98 and thereby increasing STAT3, representing a potentially new strategy to improve CPC-based therapy for MI.
机译：背景/目的褪黑激素具有许多生物活性，例如抗氧化剂和抗衰老。心脏祖细胞（CPC）已成为一种有前景的心肌梗死（MI）治疗策略。但是，梗死心肌中移植的CPCs存活率低，限制了MI治疗的成功应用。在本研究中，我们旨在研究褪黑激素是否能防止氧化应激诱导的CPCs损伤并增强其对MI的治疗功效。方法采用TUNEL法和EdU法检测褪黑激素和miR-98对H2O2诱导的细胞凋亡和增殖的影响。 MI模型用于评估褪黑激素和miR-98的潜在心脏保护作用。结果褪黑素在体外能减轻H2O2诱导的c-kit + CPCs的增殖减少和凋亡，而褪黑素预处理的CPCs与单纯的CPCs相比可显着改善梗死后心脏的功能。褪黑素能够抑制CPC中H2O2引起的miR-98水平的升高。 miR-98加剧了H2O2诱导的CPC的增殖减少和凋亡。在体内，用miR-98沉默进行CPC移植比MICC更能显着改善MI患者的心脏功能。 MiR-98靶向转录3（STAT3）的信号转导和激活物，因此加重了H2O2诱导的Bcl-2蛋白的还原。结论褪黑素预处理可通过下调miR-98从而增加STAT3来保护c-kit + CPC免受氧化应激诱导的损害，代表了改善基于CPC的MI治疗的潜在新策略。

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