Key result
Astragaloside IV attenuated lipopolysaccharide-induced cardiac dysfunction in rats and H9c2 cells by inhibiting miR-1-mediated inflammation and autophagy.
Why the study?
It was unknown whether regulation of miR-1-mediated inflammation and autophagy contributes to the protective effect of AS-IV against LPS-induced cardiac dysfunction in rats.
Does Astragaloside IV improve lipopolysaccharide-induced cardiac dysfunction in rats and H9c2 cells?
Does Astragaloside IV improve lipopolysaccharide-induced cardiac dysfunction in rats and H9c2 cells?
Astragaloside IV protects against LPS-induced cardiac dysfunction by inhibiting miR-1-mediated inflammation and autophagy in preclinical models.
AS-IV cardioprotection via miR-1 in LPS rat models is hypothesis-generating; leaves open human translation.
Introduction: . The present study was designed to investigate whether the regulation of microRNA-1 (miR-1)-mediated inflammation and autophagy contributes to the protective effect of AS-IV against cardiac dysfunction in rats treated with lipopolysaccharides (LPS). Methods: Animal model of cardiac dysfunction in rats or cellular model of injured H9c2 heart cell line was established by using LPS. Echocardiography, electron microscopy, enzyme-linked immunosorbent assay, immunofluorescence, quantitative RT-PCR, and Western blotting were used to determine the cardiac function and expression of inflammation- and autophagy-related proteins at both the mRNA and protein levels. Results: LPS caused cardiac dysfunction in rats or injury in H9c2 cells and induced inflammation and autophagy. Compared with LPS treatment, AS-IV treatment attenuated cardiac dysfunction or cell injury, accompanied by inhibition of inflammation and autophagy. However, the miR-1 mimics partly abolished the effects of AS-IV. In addition, the effect of the miR-1 inhibitor was similar to that of AS-IV in the LPS model. Further analyses showed that AS-IV treatment decreased the mRNA expression of miR-1 in the heart tissue of rats and H9c2 cells treated with LPS. Conclusion: These results suggest that AS-IV attenuated cardiac dysfunction caused by LPS by inhibiting miR-1-mediated inflammation and autophagy, thereby providing a novel mechanism for the protection against cardiac diseases.
No takes yet. Share an insight, caveat, or question.
Wang et al. (2022) studied Lipopolysaccharide-induced cardiac dysfunction. Astragaloside IV (AS-IV) vs. LPS treatment alone was evaluated on Cardiac dysfunction, inflammation, and autophagy. Astragaloside IV attenuated lipopolysaccharide-induced cardiac dysfunction in rats and H9c2 cells by inhibiting miR-1-mediated inflammation and autophagy.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: