Astragaloside IV Attenuates – In the LPS-induced ARDS

In the LPS-induced ARDS cellular model, the cellular viability of highly regulated astragaloside IV, SOD activity and ZO-1 and LC3B I expressions, but with regulated cellular apoptosis, TNF-α, IL-6, LC3B II, Beclin-1 and atg5, as well as LDH and MDA expressions. CONCLUSIONS: Astragaloside IV may, directly or indirectly, suppress the onset of autophagy, suppress oxidative stress and inflammatory response, further improve cell viability and close binding and reduce apoptosis in the endothelial lung cell model stimulated by ARDS, thereby increasing therapeutic function in ARDS. RESULTS: LPS effectively inhibited cell viability and expression of LC3B I and improved expression of LC3B II, Beclin-1 and atg5 in MLE-12 cells. Astragaloside IV inhibits cell viability and ZO-1 expression after rape treatment. Astragaloside IV suppresses pulmonary epithelial cell damage caused by lipopolysaccharides, thereby inhibiting autophagy. Astragaloside IV reduces lipopolysaccharide damage to lung epithelial cells by inhibiting autophagy. Cell viability was estimated using the cell number kit 8 and cell apoptosis using flow cytometry. It is recommended to consult a licensed physician before carrying out any natural, integrative or conventional treatment. METHODS: MLE-12 cells were induced by the LPS to build an in vitro ARDS model. By providing the information in this document, we do not diagnose, treat, cure, mitigate or prevent any disease or medical condition.

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