5.3 Heart
As one of the main damaged organs during sepsis, the heart can develop into infectious myocarditis when it is infected by the outside world, resulting in cardiac insufficiency and heart failure, which is also one of the main causes of death of hospitalized patients with sepsis in ICU[56]. Other studies have shown that ventricular muscle is inhibited in sepsis, which is manifested as diastolic dysfunction [57,58]. Wang[59] et al. Preliminarily screened the core target of retinoic acid (RA) against sepsis through network pharmacology, and then established a mouse sepsis model to observe the survival, cardiac function, and antioxidant level of mice. The results showed that RA can improve the survival rate and cardiac function of septic mice, which may be through regulating the PI3K Akt signaling pathway and key gene expression to reduce lipopolysaccharide-induced cardiac dysfunction. Wu[60] et al. Applied network pharmacology to predict the potential target and molecular mechanism of epigallocatechin gallate (EGCG) in the treatment of septic cardiomyopathy. The experimental results showed that EGCG improved myocardial injury in septic cardiomyopathy through anti-inflammatory and anti-apoptotic mechanisms.