Search

BACKGROUND: Corona Virus Disease 2019 (COVID-19) is a highly contagious, rapidly variable, and dangerous infectious disease. However, no specific and effective treatment for COVID-19 is available until now. The safety and efficacy of mesenchymal stem cells and their exosomes have been well verified in numerous clinical trials. Their immunomodulatory and tissue regeneration capabilities may support them as a prospective therapy for COVID-19 application in the clinic. OBJECTIVE: To focus on the development, pathogenesis and the current treatment status of COVID-19, efficacy and possible immunomodulatory mechanisms of mesenchymal stem cells and their exosomes for COVID-19 so as to provide new insights into the clinical treatment for the disease in the future. METHODS: Articles were searched on PubMed and CNKI with the key words of “SARS-CoV-2, COVID-19, cytokine storm, acute respiratory distress syndrome, mesenchymal stem cells, exosomes, immune regulation, tissue repair” in Chinese and English. Finally, 64 articles were collected for this review. RESULTS AND CONCLUSION: Acute respiratory distress syndrome and acute lung injury caused by cytokine storm are the primary precipitating factors of death in individuals with COVID-19. Mesenchymal stem cells and their exosomes can effectively treat the symptoms of acute respiratory distress syndrome and repair the damaged lung tissue in COVID-19 patients by reducing the cytokine storm and promoting the regeneration of alveolar epithelial cells through the interaction with immune cells and their paracrine effects. All of these investigations confirmed that mesenchymal stem cells and their exosomes can fight the COVID-19 infection, and this might be a promising, safe and effective strategy. However, more preclinical studies and randomized, controlled clinical trials are needed to conduct the biodistribution, metabolic fate, and the potential treatment risks of mesenchymal stem cells and their derived exosomes in vivo to fully exploit their clinical efficacy. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the mechanism of Liangge Powder inhibiting cytokine storm in acute lung injury ( ALI) based on network pharmacology and molecular docking. METHODS: The active ingredients and action targets of Liangge Powder were screened from the traditional Chinese medicine systems pharmacology database and analysis platform; the disease targets of ALI were obtained from online mendelian inheritance in man, Gene Cards and other medical databases. Uniprot database was used to query the genes corresponding to the targets, R software and String database were adopted to construct protein-protein interaction ( PPI) network, Cytoscape software was used to construct herbal-compound-target interaction network, R software was used to perform gene ontology (GO) function enrichment analysis and Kyoto encyclopedia of genes and genomes ( KEGG) pathway enrichment analysis, so as to predict the molecular mechanisms. Autodock Vina software was adopted to conduct molecular docking on the core components of Liangge Powder with IL-I~, IL-6, TNF-a receptors and glycogen synthase kinase 3~. RESULTS: Totally 149 active ingredients and 23 7 targets were found in Liangge Powder in the treatment of ALI, the key targets involving AKTI, IL-6 and MAPK3, etc. ; the GO functional enrichment was mainly biological processes, including oxidative stress, lipopolysaccharide response and bacteriogenic molecule, etc. The KEGG pathway mainly involved PI3K-Akt, AGE-RAGE and TNF pathways, etc. ; results of molecular docking showed that the binding forces of core compounds, such as phillyrin, stigmasterol, glabridin, pterocarpin and quercetin, was similar to that of clinically used anti-inflammatory drugs, among which phillyrin was the strongest. CONCLUSIONS: Liangge Powder may act on targets and pathways of AKTl, IL-6, PI3K-Akt and AGE-RAGE through various active ingredients such as phillyrin and and quercetin, and exert therapeutic effects on ALI in terms of anti-inflammatory, antibacterial, antioxidant and immunoregulation. [ABSTRACT FROM AUTHOR]