2017
DOI: 10.1248/bpb.b16-00329
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Hydroxysafflor Yellow A Alleviates Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Mice

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Cited by 22 publications
(19 citation statements)
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“…The results suggested that HSYA has protective effects in dopaminergic neurons induced by LPS, and the mechanisms may be associated with the inhibition of inflammatory responses [62]. HSYA (14,28, and 56 mg/kg) was intraperitoneally injected to review lipopolysaccharide (LPS)-induced acute respiratory distress syndrome in mice [63]. Safflower yellow (SY) was shown to exert an anti-inflammatory effect on BV2 microglia [64].…”
Section: Anti-inflammatory Effectsmentioning
confidence: 99%
“…The results suggested that HSYA has protective effects in dopaminergic neurons induced by LPS, and the mechanisms may be associated with the inhibition of inflammatory responses [62]. HSYA (14,28, and 56 mg/kg) was intraperitoneally injected to review lipopolysaccharide (LPS)-induced acute respiratory distress syndrome in mice [63]. Safflower yellow (SY) was shown to exert an anti-inflammatory effect on BV2 microglia [64].…”
Section: Anti-inflammatory Effectsmentioning
confidence: 99%
“…To treat ALI mice, SYA (ChromaDex, Irvine, CA, USA), HSYA (Santa Cruz, Dallas, TX, USA) and AHSYB (Nature Standard, Shanghai, China) was dissolved in saline and intraperitoneally administered immediately after the injection of LPS. All these three compounds were given at 5 × 10 -5 mol/kg in 400 μl saline [17]. The materials required for the experiment were obtained after 24 hours.…”
Section: In Vivo Experimentsmentioning
confidence: 99%
“…The further investigation demonstrated that intraperitoneal injection of LPS to the mice resulted in upregulation of protein expressions of TLR4, myeloid differentiation factor 88 (MyD88) and Toll/IL-1 receptor- (TIR-) domain-containing adapter-inducing interferon- β (TRIF) and phosphorylation of MAPKs, translocation of NF- κ B/p65, and downregulation of I κ B- α , all of which could be deteriorated by HSYA [ 77 ]. Zhang et al observed the negative influence of HSYA on the binding of LPS to the cell membrane receptor in the LPS-caused ARDS mice model [ 78 ]. And injection of HYSA alleviated the mRNA and protein levels of Col I, type III collagen (Col III), α -SMA, myeloid differentiation-2 (MD-2), and cluster of differentiation 14 (CD14) as well as inflammatory factors in plasma or lung and the collagen deposition in lung via suppressing the TLR4/NF- κ B pathway.…”
Section: Pharmacologymentioning
confidence: 99%
“…And injection of HYSA alleviated the mRNA and protein levels of Col I, type III collagen (Col III), α -SMA, myeloid differentiation-2 (MD-2), and cluster of differentiation 14 (CD14) as well as inflammatory factors in plasma or lung and the collagen deposition in lung via suppressing the TLR4/NF- κ B pathway. The in vivo test demonstrated the inhibitory effect of HYSA on the specific binding of LPS to receptors on A549 or Eahy926 cell membranes, suggesting the TLR4 receptor a target of HSYA on the cell membrane [ 78 ].…”
Section: Pharmacologymentioning
confidence: 99%