Fig. 6

Ang-(1–7) inhibits inflammatory response, mitochondrial dysfunctioning, and oxidative stress, in LPS-induced H9c2 cells. A The H9c2 cell viability, after being pretreated with varying concentrations of Ang-(1–7) (10^–6, 10^–7, 10^–8 mol/L) for 12 h, was measured using the CCK8 assay (n = 6). B The H9c2 cell viability after Ang-(1–7) (10^–6, 10^–7, 10^–8 mol/L) pretreatment for 1 h before LPS stimulation for 12 h was measured using the CCK8 assay (n = 6). C IL-1β protein concentration in the H9c2 cells (n = 6). D–F The IL-1β, TNF-α, and IL-6 mRNA expression levels in H9c2 cells (n = 4). G, H TNF-α and IL-6 protein concentrations in H9c2 cells (n = 6). I, J Quantitative analysis and flow cytometry histograms depicting the ROS production in H9c2 cells (n = 6). K, L Quantitative analysis and flow cytometry plots describing the ratio of monomer JC-1 cells (representing mitochondrial damage) in every group (n = 4). Cells with monomeric JC-1 were green in the P2 region, representing damaged mitochondria. B ^*p < 0.05 than control, ^#p < 0.05 than LPS mice. D–L Ang-(1–7) intervention using the pretreatment concentration of 10^–6 mol/L for 1 h, and LPS activation of 1 ug/mL for 12 h. NS: no significant difference, ^*p < 0.05, ^**p < 0.01, ^***p < 0.001