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.
Background Acute respiratory distress syndrome (ARDS) is a life-threatening respiratory disease and its treatment is not fully established. Triptolide, one of Tripterygium wilfordii’s main active components, has been proved to alleviate Lipopolysaccharide (LPS)-induced ARDS. Imbalance of MicroRNAs (miRNAs) is recognized as the pathogenic mechanism of various diseases, including ARDS. However, the specific miRNAs that play a key regulatory role in the anti-inflammatory effect of triptolide in ARDS remain elusive. Methods In this study, we administered triptolide in a mouse model of ARDS, and whole transcriptome sequencing was applied to identify meaningful miRNAs and validate them in vitro. Results The results showed that triptolide may reduce the inflammatory response in ARDS by regulating miR-9-5p. The data further proved that LRG1 and CLDN5 expression are regulated by miR-9-5p, and triptolide can down-regulate the expression of miR-9-5p by regulating negatively the expression of LRG1 and CLDN5. Conclusion Our study revealed that miR-9-5p was the specific miRNAs that plays key role in triptolide’s alleviation of ARDS inflammation by regulating target genes, and its inhibitory effect on LRG1 and CLDN5 expression was verified.
Background: Acute respiratory distress syndrome (ARDS) is a life-threatening respiratory disease and its treatment is not fully established. Triptolide, one of Tripterygium wilfordii’s main active components, has been proved to alleviate Lipopolysaccharide (LPS)-induced ARDS. Imbalance of MicroRNAs (miRNAs) is recognized as the pathogenic mechanism of various diseases, including ARDS. However, the specific miRNAs that play a key regulatory role in the anti-inflammatory effect of triptolide in ARDS remain elusive.Methods: In this study, we administered triptolide in a mouse model of ARDS, and whole transcriptome sequencing was applied to identify meaningful miRNAs and validate them in vitro. Results: The results showed that triptolide may reduce the inflammatory response in ARDS by regulating miR-9-5p. The data further proved that LRG1 and CLDN5 expression are regulated by miR-9-5p, and triptolide can down-regulate the expression of miR-9-5p by regulating negatively the expression of LRG1 and CLDN5.Conclusion: Our study revealed that miR-9-5p was the specific miRNAs that plays key role in triptolide’s alleviation of ARDS inflammation by regulating target genes, and its inhibitory effect on LRG1 and CLDN5 expression was verified.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.