Compound Astragalus Oral Liquid Attenuates Ventricular Remodeling in Heart Failure After Myocardial Infarction via the AMPK/TGF‐ β /Smad Signaling Pathway

Figures

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  Figure 1. UPLC‐Q‐TOF/MS analysis of CAOL. (A) Base peak chromatogram, positive ion mode. (B) Base peak chromatogram, negative ion mode.

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  Figure 2. CAOL improves cardiac function and attenuates pathological remodeling and myocardial injury in AMI‐HF rats. (A) Representative M‐mode echocardiographic images. (B–D). Quantification results of LVIDs, LVIDd, and LVEF (n = 8). (E) Representative images of H&E staining. Scale bar = 200 μm. (F) Representative images of Masson trichrome staining, blue stain represents fibrous tissue and collagen deposition. Scale bar = 200 μm. (G) Representative images of TUNEL staining. Scale bar = 200 μm. (H) The heart weight/body weight ratio of rats (n = 8). (I) Collagen volume fraction of Masson trichrome staining (n = 5). (J) Quantification of TUNEL‐positive staining (n = 5). Data were shown as mean ± SD, # p < 0.05, ## p < 0.01 compared with the sham group. ∗p < 0.05, ∗∗p < 0.01 compared with the model group, ns means nonsignificant.

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  Figure 3. Systemic effects of CAOL on circulating biomarkers of inflammation and oxidative stress. (A) IL‐6, (B) IL‐10, (C) TNF‐α, (D) IFN‐γ, (E) SOD, and (F) MDA levels with administration of CAOL in serum were analyzed. Data were shown as mean ± SD (n = 6), ## p < 0.01 compared with the sham group. ∗p < 0.05, ∗∗p < 0.01 compared with the model group, ns means nonsignificant.

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  Figure 4. Network pharmacology analysis reveals potential targets and mechanisms of CAOL against AMI‐HF. (A) Venn diagram of compound targets shared by CAOL and AMIHF. (B) The PPI network of intersection targets and topological screening process of the active ingredient−target−disease network diagram. (C) GO enrichment analysis of the anti‐AMIHF targets of CAOL. (D) KEGG enrichment analysis for anti‐AMIHF targets of CAOL.

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  Figure 5. CAOL enhances AMPK activity and suppresses the TGF‐β/Smad pathway in myocardial tissue. (A–D) The mRNA levels of AMPK, TGF-β, SMAD2, and SMAD3 were detected, respectively, by RT‐qPCR (n = 6). (E–L) WB analysis and quantification of the protein levels of AMPK, p‐AMPK, TGF‐β1, Smad2, p‐Smad2, Smad3, and p‐Smad3 (n = 6). Data were shown as mean ± SD, ## p < 0.01 compared with the sham group. ∗p < 0.05, ∗∗p < 0.01 compared with the model group, ns means nonsignificant.