Key result
Andrographolide ameliorates aortic valve incrassation and calcification by inhibiting valve interstitial cell proliferation via the MAPK-ERK signaling pathway.
Why the study?
Cell proliferation changes at the initial stage of calcific aortic valve disease represent an important therapeutic target, prompting investigation into whether andrographolide can inhibit valve interstitial cell proliferation to delay disease progression.
Does andrographolide reduce cell proliferation and calcification in models of calcific aortic valve disease?
Does andrographolide reduce cell proliferation and calcification in models of calcific aortic valve disease?
p-value: p=<0.05
Andrographolide ameliorates calcific aortic valve disease progression in preclinical models by inhibiting valve interstitial cell proliferation via the MAPK-ERK pathway.
Does not support clinical use of andrographolide in aortic valve disease; leaves open translation from animal models to patients.
Calcific aortic valve disease (CAVD) is an active pathobiological process that involves fibrosis and calcification of aortic valve leaflets, thereby causing cardiac hemodynamic changes and eventually heart failure. Cell proliferation changes at the initial stage of CAVD are an important target for pharmaceutical intervention. This study aimed to investigate whether andrographolide (AGP) could inhibit the proliferation of valve interstitial cells (VICs) in vitro and in vivo to delay the process of CAVD. Cell proliferative factors were tested in both healthy and CAVD aortic valve samples. Cell cycle, cell growth, and calcification of VICs were assessed using flow cytometry, CCK8 assay, EdU staining, and Alizarin Red S staining. The expression of cell proliferative factors and osteogenic factors were quantified by qRT-PCR or immunofluorescence staining. The interaction between AGP and ERK (extracellular regulated protein kinases) was detected by molecular docking. In addition, a high-fat diet-fed animal model was used to verify the effect of AGP on CAVD in vivo . In conclusion, we found that AGP ameliorates aortic valve incrassation by inhibiting cell proliferation via the MAPK-ERK signaling pathway. Therefore, AGP is a promising drug that prevents the occurrence of CAVD via regulating cell proliferation.
No takes yet. Share an insight, caveat, or question.
Huang et al. (2022) studied Calcific Aortic Valve Disease. Andrographolide vs. Control (vehicle/DMSO) was evaluated on Cell proliferation and aortic valve incrassation/calcification (p=<0.05). Andrographolide ameliorates aortic valve incrassation and calcification by inhibiting valve interstitial cell proliferation via the MAPK-ERK signaling pathway.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: