首页> 外文期刊>Journal of tissue engineering and regenerative medicine >Curcumin reverses diabetes‐induced endothelial progenitor cell dysfunction by enhancing MnSOD expression and activity in vitro and in vivo
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Curcumin reverses diabetes‐induced endothelial progenitor cell dysfunction by enhancing MnSOD expression and activity in vitro and in vivo

机译:姜黄素通过在体外和体内增强MNSOD表达和活性来逆转糖尿病诱导的内皮祖细胞功能障碍

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Abstract Diabetes mellitus (DM) causes dysfunction of endothelial progenitor cells (EPCs), resulting in impaired wound healing. EPC therapy is a potential substitute to the current treatments of chronic wounds. Because EPCs isolated from diabetic patients are dysfunctional and therefore pose an obstacle in their efficacious employment in autologous cell therapy, a strategy to rescue them prior to transplantation would be expected to improve the efficacy of autologous cell therapy multifold. Compromised reactive oxygen species scavenging ability being the main cause of EPC dysfunction (EPCD), reactive oxygen species scavengers are likely to reverse or rescue EPCD. Therefore, in this study, we evaluated the potential of curcumin in reversing DM‐induced EPCD. We found that in vitro treatment of bone marrow EPCs from diabetic mice (D‐EPC) with curcumin restored their functionality, as judged by colony formation, tubule formation, and migration assays. Most importantly, autologous transplantation of curcumin‐treated D‐EPCs onto diabetic wounds also resulted in accelerated wound healing. Furthermore, curcumin‐treated diabetic mice exhibited improved wound healing, as compared with their vehicle‐treated diabetic counterparts, underscoring the efficacy of curcumin in vivo as well. The levels and activity of manganese superoxide dismutase (MnSOD) in D‐EPCs treated in vitro with curcumin or those isolated from curcumin‐treated diabetic mice were comparable with those in non‐diabetic EPCs. Addition of methyl mercury chloride to inhibit MnSOD activity during curcumin treatment abolished the salutary effects of curcumin. Our data demonstrate that curcumin reverses DM‐induced EPCD by boosting MnSOD expression and activity and emphasizes its potential for use in autologous cell therapy for diabetic wound management.
机译:摘要糖尿病(DM)导致内皮祖细胞(EPC)的功能障碍,导致伤口愈合受损。 EPC疗法是对当前慢性伤口治疗的潜在替代品。因为从糖尿病患者分离的EPCS具有功能失调,因此在其在自体细胞疗法中有效的就业构成障碍,预期在移植之前拯救它们的策略来提高自体细胞治疗多型的疗效。受到影响的反应性氧物种清除能力是EPC功能障碍(EPCD)的主要原因,反应性氧物种清除剂可能会逆转或救出EPCD。因此,在本研究中,我们在逆转DM诱导的EPCD中评估了姜黄素的潜力。我们发现,通过含污染物形成,小管形成和迁移测定判断,从糖尿病小鼠(D-EPC)的骨髓EPC的体外处理恢复其功能。最重要的是,将姜黄素处理的D-EPC的自体移植到糖尿病伤口中也导致伤口愈合加速。此外,姜黄素处理的糖尿病小鼠表现出改善的伤口愈合,与其载体处理的糖尿病患者相比,抑制姜黄素在体内的疗效。用姜黄素或姜黄素处理的糖尿病小鼠分离的体外处理的D-EPCs中锰超氧化物歧化酶(MNSOD)的水平和活性与非糖尿病EPC中的那些相当。添加甲基汞氯化甲基汞以抑制姜黄素治疗期间的MNSOD活性废除了姜黄素的良效应。我们的数据表明,姜黄素通过提高MNSOD的表达和活性来反转DM诱导的EPCD,并强调其用于糖尿病伤口管理的自体细胞治疗的可能性。

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