Research Paper Volume 13, Issue 11 pp 15151—15163

Narciclasine attenuates sepsis-induced myocardial injury by modulating autophagy

Narciclasine attenuates LPS-induced cardiomyocyte inflammation. (A) The viability of cardiomyocytes treated with different concentrations of narciclasine (0, 30, 100, and 300 nM) was measured by CCK8 assays. (B) The viability of cardiomyocytes stimulated with LPS and treated with different concentrations of narciclasine (0, 30, 100, and 300 nM) was measured by CCK8 assays. (C–E) The concentration of inflammatory cytokines (TNF-α, IL-1β, and IL-6) in cardiomyocytes stimulated with LPS and treated with different concentrations of narciclasine (0, 30, 100, and 300 nM) was measured by ELISA kits. (F) Quantification of LPS-induced neonatal rat cardiomyocyte apoptosis was analyzed by FACS. n = 3 per group. Data represent the mean ± SEM. *P #P

Figure 1. Narciclasine attenuates LPS-induced cardiomyocyte inflammation. (A) The viability of cardiomyocytes treated with different concentrations of narciclasine (0, 30, 100, and 300 nM) was measured by CCK8 assays. (B) The viability of cardiomyocytes stimulated with LPS and treated with different concentrations of narciclasine (0, 30, 100, and 300 nM) was measured by CCK8 assays. (CE) The concentration of inflammatory cytokines (TNF-α, IL-1β, and IL-6) in cardiomyocytes stimulated with LPS and treated with different concentrations of narciclasine (0, 30, 100, and 300 nM) was measured by ELISA kits. (F) Quantification of LPS-induced neonatal rat cardiomyocyte apoptosis was analyzed by FACS. n = 3 per group. Data represent the mean ± SEM. *P < 0.05 vs. the PBS group. #P < 0.05 vs. the LPS group.