Fig. 7: Galangin 3-methyl ether (G3-ME) prevents pathological cardiac hypertrophy by directly targeting HDAC2. | Acta Pharmacologica Sinica

Fig. 7: Galangin 3-methyl ether (G3-ME) prevents pathological cardiac hypertrophy by directly targeting HDAC2.

From: Galangin 3-methyl ether alleviates mouse hypertrophic cardiomyopathy via targeting HDAC2 and subsequently inactivating the PI3K-AKT signaling pathway

Fig. 7: Galangin 3-methyl ether (G3-ME) prevents pathological cardiac hypertrophy by directly targeting HDAC2.

a The flowchart of network pharmacology and the protein-protein interaction diagram. b KEGG enrichment analysis according to 42 potential targets of G3-ME. c The binding energy between G3-ME and potential targets enriched in the PI3K-AKT signaling pathway. d Representative schematic diagram of molecular docking between HDAC2 and G3-ME. e Schematic diagram of HDAC2 regulating the PI3K-AKT signaling pathway. f, g The protein expression levels of p-HDAC2 and HDAC2 in H9c2, hESC-CMs and cardiac tissues of wild-type (WT) or Myh6R404Q mice. n = 4 per group. h Drug affinity reaction target stability (DARTs) assay was performed in vitro and in vivo on H9c2. i DARTs assay was performed in vitro and in vivo on hESC-CMs. j Cellular thermal shift assay was performed on H9c2 and hESC-CMs, respectively. k The results of surface plasmon resonance indicated a direct binding interaction between G3-ME and HDAC2, with a binding affinity of 3.36 μM. The values are mean ± SEM. *P < 0.05.

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