[Plumbagin protect against sepsis-induced myocardial injury in mice by inhibiting the JAK2/STAT3 signaling pathway to reduce cardiomyocyte pyroptosis].
Year: 2024
Type: other
Abstract: OBJECTIVE: To explore the mechanism of plumbagin for protecting against sepsis-induced myocardial injury in mice. METHODS: Network pharmacology analysis was used to obtain the key targets of plumbagin and diseases, which were subjected to GO and KEGG analysis, and the binding energy was verified using molecular docking. In a mouse model of cecal ligation and puncture (CLP), the protective effect of plumbagin treatment prior to CLP against sepsis-induced myocardial injury was evaluated by examination of myocardial function and pathology using echocardiography and HE staining. Serum levels of CK-MB, LDH, MDA, IL-1β and IL-18 and myocardial ROS level in the mice were detected, and Western blotting was used to determine the protein expression levels of STAT3, GSDMD, caspase-11, JAK2, P-STAT3, P-JAK2, GSDMD-N and HMGB1 in the myocardial tissues. RESULTS: < 0.05). Pretreatment with plumbagin significantly improved cardiac functions of CLP mice, lowered serum levels of CK-MB, LDH, MDA, inflammatory factors and myocardial ROS, and decreased the expression levels of JAK2/STAT3 signaling pathway and pyroptosis-related proteins. CONCLUSION: Plumbagin pretreatment alleviates myocardial injury in septic mice possibly by inhibiting the STAT3 signaling pathway to reduce cardiomyocyte pyroptosis.
Source: PubMed
Institution: Bengbu Medical College
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W4405028445