Analysis of Therapeutic Targets of A Novel Peptide Athycaltide-1 in the Treatment of Isoproterenol-Induced Pathological Myocardial Hypertrophy

Figures

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  Figure 1. HE staining, Masson staining, and protein expression of ANP and BNP. (a) The cross-section of the cardiac tissue (the magnification is 20.0x) by HE staining in each group (n = 3). (b) The cross-section of the cardiac tissue (the magnification is 20.0x) by Masson staining in each group (n = 3). (c) The protein expression of ANP and BNP in each group (n = 3). ∗P < 0.05 and ∗∗P < 0.01.

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  Figure 2. (a) Histogram of upregulated and downregulated DEPs. Upregulated DEPs were in grey, and downregulated DEPs were in yellow. (b) The heatmap and cluster analysis of DEPs. Upregulated DEPs were in red, and downregulated DEPs were in green. (c) Volcano plot representation of DEPs. A: upregulated proteins; B: downregulated proteins; and C: unchanged proteins. (d) GO enrichment and KEGG analysis of DEPs in the ISO/control and (e) ATH-1/ISO comparisons. The top 10 terms of BP, MF, CC, and KEGG analysis were displayed with the parameter protein count and P value. (f) Mapping of DEPs onto a composite network based on predicted protein-protein interaction. A predicted PPI network has been visualized for the identified DEPs.

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  Figure 3. ATH-1 decreased the protein expression of Hspa1, p-ERK, p-JNK, and p-p38 in hypertrophic myocardium and enhanced the activity of T-SOD. (a) Differentially abundant proteins identified in the iTRAQ experiment. (b) The protein expression of Hspa1 (n = 3). ∗P < 0.05 and ∗∗P < 0.01. (c) The activity of T-SOD in each group (n = 3). ∗∗P < 0.01 and ∗∗∗P < 0.001. (d) The protein expression of ERK1/2 and p-ERK1/2 (n = 3). ns indicates none significance, ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001. (e) The protein expression of JNK and p-JNK (n = 3). ns indicates none significance, ∗P < 0.05. (f) The protein expression of p38 MAPK and p-p38 MAPK (n = 3). ns indicates none significance, ∗P < 0.05 and ∗∗∗P < 0.001.