The peptide compound urantide regulates collagen metabolism in atherosclerotic rat hearts and inhibits the JAK2/STAT3 pathway

Figures

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  Figure 1.. Experimental design. The setting of the experimental group, the interventions of each group and the intervention time. AS, atherosclerosis; w, weeks; d, days; n, number.

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  Figure 2.. Histological changes in the thoracic aortas of atherosclerotic rats induced by a high-fat diet identified by hematoxylin and eosin staining. In the normal group, the arterial intima was intact and smooth, and the cells were orderly arranged. In the AS model group, atherosclerotic plaque of the intima was present and the arrangement of the cells was disordered. Scale bars, 100 µm. AS, atherosclerosis.

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  Figure 3.. Alleviation of heart disease in rats with AS following urantide treatment. The following cardiac parameters improved with treatment time: (A) Pathological symptoms, (B) collagen expression, (C) cardiac pathological injury score, and (D) myocardial collagen volume. Scale bar, 50 µm. *P<0.05, **P<0.01 vs. the normal group; #P<0.05, ##P<0.01 vs. the AS model group; ^P<0.05, ^^P<0.01 vs. the simvastatin group. Data are presented as the mean ± SEM (n=6–8 rats in each group). H&E, hematoxylin & eosin; AS, atherosclerosis.

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  Figure 4.. Effect of urantide on UII/GPR14, the JAK2/STAT3 pathway and collagen metabolism in the cardiac tissue of rats with AS. Changes in the expression of the following genes and proteins with increasing drug administration time: (A) relative expression level of genes. Changes in the expression of the following genes and proteins with increasing drug administration time: (B-a) relative expression level of signaling pathway proteins, (B-b) relative expression level of collagen metabolism related proteins and (C) MMP-2/TIMP-2 protein ratio. *P<0.05, **P<0.01 vs. the normal group; #P<0.05, ##P<0.01 vs. the AS model group; ^P<0.05, ^^P<0.01 vs. the simvastatin group. Data are presented as the mean ± SEM (n=6–8 rats in each group). AS, atherosclerosis; UII, urotensin II; G protein-coupled receptor 14; JAK2, Janus kinase 2; p, phosphorylated; STAT3, signal transducer and activator of transcription 3; MMP-2, matrix metalloproteinase 2; TIMP-2, TIMP metallopeptidase inhibitor 2.

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  Figure 5.. Effect of urantide on the distribution and localization of p-JAK2/p-STAT3 and collagen type I/III. Immunofluorescence staining of: (A) p-JAK2, (B) p-STAT3, (C) collagen I and (D) collagen III indicating the location and intensity of the positive expression of these proteins in cardiac tissue derived from each group. Scale bars, 50 µm. Blue, nucleus; green, positive expression. AS, atherosclerosis; p-JAK2, phosphorylated-Janus kinase 2; p-STAT3, phosphorylated-signal transducer and activator of transcription 3.