Journal: Dose-Response

Article Title: 4,8-Dicarboxyl-8,9-Iridoid-1-Glycoside Alleviates Cardiac Dysfunction After Myocardial Ischaemia-Reperfusion Injury by Activating the PI3K/AKT Pathway

doi: 10.1177/15593258261444840

Figure Lengend Snippet: BIG improves cardiac function after I/RI by inhibiting the inflammatory response and myofibroblast fibrosis. (A, B, C, D, E, F, H and I) The relative expressions of MMP2, MMP9, TNF‒α, IL-1β, IL-6, BCL-2, BAX and c-caspase-3 (n=6). (G) WB results showing the expression of related proteins. (J) Representative microphotographs of TUNEL (blue, DAPI; green, TUNEL‒positive cardiomyocytes) staining of cardiomyocytes (n= 6). Scale bar: 20 μm. (K) The number of TUNEL‒positive cells represents the apoptosis rate in Sham, I/RI and BIG treated mice (n= 6). (L and M) The number of Col6a3- and TGF‒β‒positive myofibroblasts in the myocardial infarction area (n= 6). (N) Immunofluorescent colocalization of Col6a3, TGF‒β and vimentin in mice subjected to Sham, I/RI or BIG treatment (red, Col6a3 or TGF‒β; green, VIM; blue, DAPI). Scale bar: 50 μm. (O) Immunofluorescent colocalization of Col6a3, TGF‒β and TNNI3 in mice subjected to Sham, I/RI and BIG treatment (red, Col6a3 or TGF‒β; green, TNNI3; blue, DAPI). Scale bar: 50 μm. (P and Q) The number of Col6a3- and TGF‒β‒positive cardiomyocytes in the myocardial infarction area (n= 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

Article Snippet: The blocking solution was removed, and the myocardial cells were treated with primary antibodies against TNNI3 (1:50) (Bioss, BD-PE0227), Col6a3 (1:100) (Bioss, bs-0553R), and TGF-β (1:200) (Affinity, AF1027); the myocardial fibroblasts were then treated with primary antibodies against vimentin (1:100) (Bioss, BD-PE1985), Col6a3 (1:100), and TGF-β (1:200).

Techniques: Expressing, TUNEL Assay, Staining

Journal: Dose-Response

Article Title: 4,8-Dicarboxyl-8,9-Iridoid-1-Glycoside Alleviates Cardiac Dysfunction After Myocardial Ischaemia-Reperfusion Injury by Activating the PI3K/AKT Pathway

doi: 10.1177/15593258261444840

Figure Lengend Snippet: Changes in the multiomic map after myocardial infarction. (A) UMAP of the snRNA‒seq data from all the samples (n = 191,795). (B) Differential expression of Col6a3 in cardiac fibroblasts (n = 47,309) and cardiomyocytes (n = 64,510). (C) Volcano plot of the expression of all genes in myocardial fibroblasts and cardiomyocytes in the infarct area. Red, upregulated; green, downregulated; grey, no difference. (D) KEGG of differentially expressed genes. (E) The expressions of Col6a3 and TGF‒β in the myocardial tissue of the infarct area in the Sham, I/RI, and BIG treated mice (n = 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

Article Snippet: The blocking solution was removed, and the myocardial cells were treated with primary antibodies against TNNI3 (1:50) (Bioss, BD-PE0227), Col6a3 (1:100) (Bioss, bs-0553R), and TGF-β (1:200) (Affinity, AF1027); the myocardial fibroblasts were then treated with primary antibodies against vimentin (1:100) (Bioss, BD-PE1985), Col6a3 (1:100), and TGF-β (1:200).

Techniques: Quantitative Proteomics, Expressing