Key result
Andrographolide attenuated calcification of human aortic valve interstitial cells and downregulated ALP and RUNX2 via inhibition of the NF-κB/Akt/ERK pathway.
Why the study?
Calcific aortic valve disease is initiated by valve interstitial cells driving leaflet thickening and calcification, but whether andrographolide could attenuate human valve interstitial cell calcification was unknown.
Does andrographolide inhibit calcification in human valve interstitial cells?
Does andrographolide inhibit calcification in human valve interstitial cells?
Andrographolide attenuates calcification of human valve interstitial cells in vitro via the NF-κB/Akt/ERK pathway, suggesting potential as a therapeutic agent for calcific aortic valve disease.
Does not support clinical use in aortic stenosis; leaves open andrographolide for in vivo validation as a therapeutic target.
Calcific aortic valve disease (CAVD) is caused by valve interstitial cells (VICs) initiating the thickening and calcification of valve leaflets. The present study aimed to investigate whether andrographolide (AGP) could attenuate the calcification of human valve interstitial cells (hVICs). hVICs stimulated by osteoblastic medium (OM) were treated with or without AGP. RNA sequencing was utilized to investigate changes in gene expression. Cell growth and calcification of hVICs were assessed using a CCK8 assay and Alizarin Red S staining, respectively. The expression of the two calcification-related markers, RUNX2 and ALP, were quantified by qRT-PCR, Western blotting, and immunofluorescent staining. The results indicate that hVICs treated with OM plus AGP exhibited decreased Alizarin Red S staining compared with cells treated with OM only in addition to down-regulation of ALP and RUNX2. Mappings of differentially expressed genes (DEGs) in different groups using Venn diagrams during analysis of gene expression profiles, 653 common DEGs were identified that displayed different biological functions and signaling pathways after treatment with AGP. RELA, a core factor of the NF-κB pathway was inhibited by AGP in addition to phosphorylation of AKT and ERK1/2. Thus, AGP attenuated calcification of hVICs. These results demonstrate that AGP, a promising natural product, can attenuate the process of CAVD.
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Huang et al. (2020) studied Calcific aortic valve disease. Andrographolide (AGP) vs. Osteoblastic medium (OM) only was evaluated on Calcification of human valve interstitial cells and expression of RUNX2 and ALP. Andrographolide attenuated calcification of human aortic valve interstitial cells and downregulated ALP and RUNX2 via inhibition of the NF-κB/Akt/ERK pathway.
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