RESUMO
SARS-CoV-2, the pathogen of the COVID-19 pandemic, causes serious damage to human health and social stability. In severe COVID-19 cases, the infection triggers cytokine storm, resulting in multi-organ excessive inflammatory responses and even failure, which eventually leads to death. Recent studies have shown the activation of nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome plays an essential role in the pathogenesis of COVID-19. SARS-CoV-2 can activate NLRP3 inflammasome through several pathways, thereby inducing the release of a large number of pro-inflammatory cytokines. This article reviews the activation of NLRP3 inflammasome caused by SARS-CoV-2 infection and the possible molecular mechanisms, and summarizes the progress in targeted inhibition of NLRP3 inflammation, aiming to provide a new strategy for the treatment of SARS-CoV-2 infection.
RESUMO
Objective:To investigate the effects of Rad50-targeted inhibition on the radiosensitivity of head and neck squamous cell carcinoma cells.Methods:Rad50 in Tca8113 and OSCC-15 cells was down-regulated by siRNA.Then the cells were treated by a small dose of radiation(2 Gy),Western blot was used to detect the expression of Rad50 protein.Comet assay was used to evaluate the DNA double strand breaks(DSBs).Colony survival assay was performed to detect the survival rate of the cells.Telomere FISH was performed to assess the telomere length in the cells.Results:Target siRNA inhibited Rad50 protein expression in Tca8113 and OSCC-15 cells. siRNA combined with the radiation of 2 Gy produced more DSBs,decreased the proliferation and shortened the nucleus telomere length of the cells more than radiation treatment alone.Conclusion:The targeted inhibition of Rad50 may increase the radiosensitivity of Tca8113 and OSCC-15 cells.