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.