Safflor Yellow A Protects Beas-2B Cells Against LPS-Induced Injury via Activating Nrf2

Abstract

Acute lung injury and its severe form acute respiratory distress syndrome are lethal lung diseases. So far, effective therapy for the diseases is deficient and the prognosis is poor. Recently, it was found activating nuclear factor erythroid 2-related factor 2 could attenuate the injury including inflammation, oxidative stress, and apoptosis in those diseases. To discover novel therapy, we have evaluated safflor yellow A and explored the underlying mechanisms using Beas-2B cells injured by lipopolysaccharide. As a result, safflor yellow A could improve the viability of Beas-2B cells treated with lipopolysaccharide. Further investigations have revealed safflor yellow A suppressed oxidative stress induced by lipopolysaccharide via reducing reactive oxygen species and malondialdehyde, and elevating superoxide dismutase, catalase, and glutathione peroxidase. Meanwhile, the inflammation resulting from lipopolysaccharide was ameliorated through decreasing the pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-6. It was also found nuclear factor κB was inactivated by safflor yellow A. In addition, safflor yellow A downregulated cysteinyl aspartate specific proteinase-3 and Bcl-2-associated X protein and upregulated B-cell lymphoma-2 to inhibited apoptosis of Beas-2B cells induced by lipopolysaccharide. The activation of nuclear factor erythroid 2-related factor 2 was observed in Beas-2B cells, which was associated with the protective effects of safflor yellow A. And molecular docking elucidated safflor yellow A interacted with Kelch-like ECH-associated protein 1 to activate nuclear factor erythroid 2-related factor 2. These results can provide evidences for the discovery of novel therapy for further evaluation of safflor yellow A in the treatment of acute lung injury and acute respiratory distress syndrome. Graphical Abstract

Efficacy of Life Protection Probably from Newly Isolated Bacteria against Cisplatin-Induced Lethal Toxicity

“…In this experiment, Western blotting showed that the protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2) was noticeably upregulated in the Cis/Bact A and/or Cis/Bact B group mice ( Figure 6 A,B), suggesting that Bact A and/or Bact B might have a potential for life-protection by attenuating oxidative stresses and/or inflammatory injury via the regulation of the Nrf2 signaling pathway [ 17 ]. However, the protein expression of heme oxygenase 1 (Ho-1) was not so much upregulated, either in the Cis/Bact A or in the Cis/Bact B group mice ( Figure 6 A,C).…”

Effect of caspase inhibitors on hemodynamics and inflammatory factors in ARDS model rats

“…The inflammatory response plays an important role in ARDS, and the increased release of proinflammatory factors and the relatively insufficient amount of anti-inflammatory factors in the early stage of ARDS are the main mechanisms leading to an uncontrolled inflammatory response in ARDS 34 – 36 . A previous study showed that the lung tissue of LPS-induced ARDS model rats exhibited increased infiltration of polymorphonuclear leukocytes (PMNs), which produce and release many inflammatory factors, including IL-1α, IL-1β, IL-4, IL-6, IL-10, and TNF-α 37 . Among them, TNF-α, as the initiating factor of ARDS, represents the severity of the inflammatory response in the early stage of ARDS 38 .…”