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@#Objective To investigate whether metformin has protective effect on myocardial injury in patients with coronavirus disease 2019 (COVID-19) combined with coronary heart diseases and diabetes. Methods COVID-19 patients with coronary heart disease and diabetes who were admitted to Tongji Hospital from January 18 to April 25 in 2020 were enrolled. They were divided into a metformin group and a none-metformin group according to whether the metformin was used. The demographic characteristics, clinical symptoms, laboratory parameters, treatment and clinical outcomes of the two groups were analyzed retrospectively. Results There were 29 patients in the metformin group, 3 patients (12.0%, 3/25) suffered myocardial injury and 1 (3.4%) died of acute respiratory failure complicated by septic shock; 67 patients were in the non-metformin group and 24 (37.5%, 24/64) had myocardial injury but 15 died in hospital among whom 1 died of septic shock complicated by disseminated intravascular coagulation, 1 acute respiratory failure complicated by possible cerebral hemorrhage, 2 acute respiratory failure, 1 fulminant myocarditis, 3 acute myocardial infarction and 7 cardiac arrest. The incidence of myocardial injury (12.0% vs. 37.5%, P=0.019), hospital mortality (3.4% vs. 22.4%, P=0.034) and mortality of cardiovascular events (0.0% vs. 16.4%, P=0.049) in the metformin group were significantly lower than those in the non-metformin group. Multivariate analysis showed that the use of insulins (OR=11.235, P=0.003) was an influencing factor for in-hospital mortality of patients. The use of metformin (OR=0.154, P=0.013) was positively correlated with the myocardial injury. Conclusion When patients with coronary heart disease and diabetes are infected with COVID-19, metformin can effectively reduce myocardial damage and has a certain effect on reducing hospital mortality. Combined with clinical considerations, it is worthy of popularization.
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Objective:To prepare the production of TIGIT-Fc fusion protein using H22 cells stably integrated the gene by lentivirus vector , and to explore the immunoregulatory effect on macrophages by TIGIT-Fc.Methods: TIGIT-Fc fusion gene were constructed by molecular cloning.The fusion gene was then subcloned to plasmids contained the secretion signaling peptide .The secrected TIGIT-Fc fusion gene was inserted into the lentivirus backbone vector.The purified lentivirus vector was the used to infect the murine H22 cell line.TIGIT-Fc protein was purified by protein A column from the ascites of H 22-injected C57BL/6 mice.Macrophages stimulated by lipopolysaccharide ( LPS ) was challenged to TIGIT-Fc treatment or control.Cytokine levels was then detected by ELISA.Results: TIGIT-Fc protein was purified from the ascites of H 22-injected mice.PVR was upregulated in LPS-treated macrophages.IL-10 level was upregulated in TIGIT-Fc treated macrophages.Conclusion: TIGIT-Fc promotes the mature macrophages to secrete anti-inflammatory cytokine IL-10.