Research Paper Volume 13, Issue 11 pp 15151—15163

Narciclasine attenuates sepsis-induced myocardial injury by modulating autophagy

The JNK signaling pathway is responsible for narciclasine-mediated protection against sepsis-induced myocardial injury. (A) The expression levels of total JNK and phosphorylated JNK (p-JNK) were measured by western blotting. Mice were treated with SP600125, an inhibitor of JNK activity, prior to LPS stimulation to further investigate the role of JNK in autophagy. (B) The levels of autophagy-associated proteins, p-JNK and JNK were assessed by western blotting. (C) The LVEF and LVFS of mouse hearts after LPS challenge for 96 h were measured by echocardiography. (D) The survival rates of LPS-injected mice throughout the 96-h study period. n = 3–8 per group. The data are shown as the means ± SEM. *P #P

Figure 6. The JNK signaling pathway is responsible for narciclasine-mediated protection against sepsis-induced myocardial injury. (A) The expression levels of total JNK and phosphorylated JNK (p-JNK) were measured by western blotting. Mice were treated with SP600125, an inhibitor of JNK activity, prior to LPS stimulation to further investigate the role of JNK in autophagy. (B) The levels of autophagy-associated proteins, p-JNK and JNK were assessed by western blotting. (C) The LVEF and LVFS of mouse hearts after LPS challenge for 96 h were measured by echocardiography. (D) The survival rates of LPS-injected mice throughout the 96-h study period. n = 3–8 per group. The data are shown as the means ± SEM. *P < 0.05 vs. the PBS group. #P < 0.05 vs. the LPS group.