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山东大学学报 (医学版) ›› 2020, Vol. 58 ›› Issue (3): 32-37.doi: 10.6040/j.issn.1671-7554.0.2020.224

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间充质干细胞治疗新型冠状病毒肺炎的潜在机制和研究进展

鞠秀丽   

  1. 山东大学齐鲁医院儿科, 山东 济南 250012
  • 出版日期:2020-03-10 发布日期:2022-09-27
  • 通讯作者: 鞠秀丽. E-mail:jxlqlyy@163.com

Potential mechanism and research progress of mesenchymal stem cells in the treatment of 2019 novel coronavirus pneumonia

JU Xiuli   

  1. Department of Pediatrics, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China
  • Online:2020-03-10 Published:2022-09-27

摘要: 当前新型冠状病毒肆虐,严重危害人类健康、社会经济发展及全球医疗和公共卫生系统。新型冠状病毒传染性强,潜伏期长,疫情控制难度大,引起重症、危重症及死亡病例众多,尚缺乏有效特异性治疗。过度的免疫反应引起的细胞因子风暴是新型冠状病毒感染导致急性呼吸窘迫综合征、脓毒症休克和多器官衰竭甚至死亡的关键因素。间充质干细胞具有强大的抗炎及免疫调节功能,可抑制细胞因子风暴的发生、发展,同时亦有强大的组织损伤修复的能力,双管齐下可发挥减轻肺损伤、降低急性呼吸窘迫综合征等严重并发症发生风险,有望降低患者的死亡率。目前已启动了多项间充质干细胞治疗新型冠状病毒肺炎的相关临床研究项目,初步证实了安全性及有效性,提示具有良好临床应用前景。

关键词: 新型冠状病毒肺炎, 间充质干细胞, 免疫调节, 损伤修复, 细胞因子风暴综合征

Abstract: The current spread of 2019 novel coronavirus pneumonia(2019-nCoV)seriously endangers human health, socio-economic development, as well as the global medical and public health system. The 2019-nCoV is highly contagious and lethal, characterized by long incubation period and difficulty control. More importantly, there is no specific and effective treatment for this disease so far. The cytokine storm caused by excessive immune response is a key factor leading to acute respiratory distress syndrome, septic shock, multiple organ failure, and even death. As mesenchymal stem cells(MSCs)have powerful anti-inflammatory and immunoregulatory potentials, which can inhibit the occurrence and development of cytokine storms and repair tissue damage, MSCs are expected to reduce lung injury, severe complications and mortality. The academic institutes in China have initiated several clinical research projects on MSCs for the treatment of 2019-nCoV, and have preliminarily confirmed its safety, effectiveness and clinical prospect.

Key words: Novel coronavirus pneumonia, Mesenchymal stem cells, Immune regulation, Damage repair, Cytokine storm syndrome

中图分类号: 

  • R563.1
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