Liquiritin inhibits LPS-ATP-induced H9c2 cell inflammation damage.
Liquiritin inhibits LPS-ATP-induced H9c2 cell inflammation damage via the regulation of COX-2/NLRP3/Caspase-1 signaling pathway.
AI Summary
Key Findings
Abstract
Liquiritin (LQ) has demonstrated the ability to prevent and treat ventricular remodeling (VR) following acute myocardial infarction (AMI) in rats, however, the underlying mechanism remains unclear. LPS and ATP were utilized to establish a model of the myocardial cell inflammatory cascade. The levels of CK and LDH were measured through a colorimetric assay. The levels of IL-1β, IL-18, and cTnI were quantified by ELISA. mRNA and protein expressions of key targets were analyzed using immunofluorescence techniques, RT-qPCR and Western blotting. LQ (5, 10, 20μmol/L) reduced the levels of CK, LDH and cTnI, and decreased the mRNA expression levels of COX-2, NLRP3, Caspase-1, ASC and GSDMD. LQ or NS398 reduced the mRNA expression levels of COX-2, NLRP3, Caspase-1, ASC and GSDMD. LQ or NS398 decreased the fluorescence intensity of COX-2, NLRP3, and GSDMD. Additionally, LQ or NS398 decreased protein levels of COX-2, NLRP3, Cleaved-Caspase-1, ASC, GSDMD, and GSDMD-N. Furthermore, LQ or NS398 was found to diminish the release of IL-1βand IL-18. Interestingly, LQ reversed the protein expressions of COX-2 and NLRP3 caused by COX-2 overexpression. The intervention with LQ led to a significant reduction in the mRNA expressions of COX-2, NLRP3, Caspase-1, ASC, GSDMD, IL-1β, and IL-18. LQ inhibits myocardial cell inflammatory cascade induced by LPS and ATP, and the mechanism is related to the COX-2/NLRP3 signaling pathway.
Affiliation
Lan Zhou
External References
- PubMed ID:
- 41722265
Comments
Sign in or create a free account to join the conversation.
Sign in to commentBe the first to comment.