AI Article Synopsis

  • Research highlights that there are currently no effective low-side-effect drugs for acute lung injury.
  • Isochlorogenic acid A shows potential in reducing inflammation, oxidative stress, and pulmonary edema caused by LPS in acute lung injury.
  • This compound also prevents cell apoptosis and inhibits key signaling pathways, suggesting it could be a strong candidate for future treatments of acute lung injury.

Article Abstract

Nowadays, there is still no effective drug with small side effects for acute lung injury. Monomer of herb is promising for anti-inflammation therapy. In this study, we first investigated the possible effects of isochlorogenic acid A in acute lung injury induced by LPS. The effects of oxidant stress, pulmonary edema and inflammation factors induced by LPS were inhibited by isochlorogenic acid A. Levels of lung active markers and inflammation factors induced by LPS were reversed by isochlorogenic acid A. Isochlorogenic acid A inhibited the cell apoptosis induced by LPS. The protein expressions of Nf-κB/NLRP3 signaling pathway induced by LPS were inhibited by isochlorogenic acid A. In summary, isochlorogenic acid A reversed the effects induced by LPS in acute lung injury and is a promising monomer for therapy of acute lung injury, providing references for future research on therapy of acute lung injury.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6895519PMC

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