Skip to main content
. 2021 Dec 23;10:e60311. doi: 10.7554/eLife.60311

Figure 2. Post ischemic administration of 8C reduces the oxidative stress and cell death after I/R injury.

(A) Representative of TUNEL (green) and cTnT (red) double staining at boarder zone at 24 hr post I/R injury. Scale bar: 100 µm (B) Quantification of cardiomyocytes cell death of 12 sections (C–D) Serum cTni and CK-MB level at 24 hr post I/R. (E–F) Western blot and quantification of Bax and Bcl2 at 24 hr after I/R. (G) GSEA analysis of Kegg apoptotic pathways after I/R with and without 8C treatment. (H) ROS levels were measured by DHE staining. Scale bar: 200 µm. (I) Relative mean DHE fluorescence intensity measured by Image J. Error bars represent S.D. n = 3. *p < 0.05, **p < 0.01 vs Sham; #p < 0.05, ##p < 0.01 vs I/R group. Data were analyzed by one-way ANOVA, followed by post-hoc Tukey test.

Figure 2—source data 1. Original numeric data for Figure 2.
Figure 2—source data 2. Original western blot figure for Figure 2.

Figure 2.

Figure 2—figure supplement 1. 8C administration altered the gene expression after I/R injury.

Figure 2—figure supplement 1.

(A–B) Serum CK and LDH level at 24 hr post I/R. (C) Volcano plot of differential expressed genes in 8C-treated and saline-treated hearts after I/R. Differential expressed genes with abs(Log2Foldchange) > 1, and padj < 0.05 were labelled in red. (D) Top gene set enrichment of differential expressed genes using GO biological process gene sets. (E) Heatmap of antioxidant gene expression. (F) Quantification of myocardial SOD activity after I/R with or without I/R. n = 3, *p < 0.05 vs Sham group; #p < 0.05 vs I/R group. Data were analyzed by one-way ANOVA (B and D), followed by post-hoc Tukey test.