Research Paper Volume 14, Issue 8 pp 3617—3632
Puerarin protects against sepsis-induced myocardial injury through AMPK-mediated ferroptosis signaling
Figure 7. A hypothesis on the mechanism of Puerarin on sepsis-induced myocardial injury: the combination of LPS and TLRs promotes the body to produce a large number of inflammatory cytokines TNF-α, IL-1β, and IL-6, which affect the coupling process of the oxidative respiratory chain in the mitochondria and causes the accumulation of ROS. The accumulation of ROS can induce ferroptosis, which in turn leads to myocardial damage. However, in this study, the experimental results indicate that Puerarin may inhibit the occurrence of ferroptosis by activating AMPK, thereby exerting its cardioprotective effect.