Effects of Triptolide on Cell Viability, Secretion of Inflammatory Cytokines, and Gene Expression of Severe Coronavirus Disease 2019（COVID-19）Pseudovirus Cell Model (preprint)

ABSTRACT

Background: Acute respiratory distress syndrome (ARDS), which is caused by severe immune cell response and associated alveolar inflammation, is also a critical complication in hospitalized patients with COVID-19. Triptolide is a powerful anti-inflammatory and immunosuppressive drug and is proved to help relieve the inflammation of ARDS. However, its anti-inflammatory effect on COVID-19 patients with ARDS complications remains uncertain. Methods: In this study, human normal lung epithelial cells (BEAS-2B), the pseudovirus system of syndrome coronavirus 2(SARS-CoV-2) and lipopolysaccharide (LPS) were used to construct as severe COVID-19-pseudovirus cell model to explore the effects of triptolide on cell viability, secretion of inflammatory cytokines, and gene expression. Results: The results showed that triptolide increased cell viability, decreased the secretion levels of cytokines IL-6, TNF-a, and increased the expression of IL-10. Furthermore, transcriptome analysis in this cell models showed that the Differentially expressed genes (DEGs) were related to plasma membrane integrity, metabolic activity and mitochondrial function, and were associated with TNF, FOXO, mTOR and MAPK signaling pathways. Conclusion: Take into consideration previous studies on the functions of triptolide in BEAS-2B cells, the current study indicated that triptolide can play a critical role in protecting against inflammatory damage and maintaining the normal physiological function of BEAS-2B cells in response to pseudovirus and LPS infection.