Yellow crystalline powder
Carthamus tinctorius L.
DMSO : ≥ 34 mg/mL (55.51 mM);
1015.8±65.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:146087-19-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Hydroxysafflor yellow A (HSYA) is the main active ingredient of edible plant safflower. HSYA has demonstrated anti-inflammatory effects. The inflammatory response is the key mechanism responsible for asthma, and the pro-inflammatory platelet-activating factor (PAF) is known to play a role in the pathology of bronchial asthma. In this study, we stimulated human bronchial smooth muscle cells (HBSMCs) with PAF and examined the effects of HSYA on the resulting asthma-related process. PAF stimulation induced HBSMC activation, induced proliferation, increased expression of the pro-inflammatory cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor-α, and activated asthma-related signaling pathways. All these effects were significantly inhibited by treatment with HSYA (9, 27, 81 μmol L-1). The effects of HSYA were prevented by the addition of a PAF receptor (PAFR) antagonist or by PAFR gene silencing with small interfering RNA. These results suggest that HSYA may inhibit PAF-induced activation of HBSMCs by targeting the PAFR. Overall, these findings provide evidence that HSYA can be applied as a potential therapeutic agent in the treatment of bronchial asthma.
Hydroxysafflor yellow A (HSYA) targets the platelet-activating factor (PAF) receptor and inhibits human bronchial smooth muscle activation induced by PAF.
Guo X 1, Zheng M , Pan R , Zang B , Gao J , Ma H , Jin M .
2019 Aug 1
Hydroxysafflor Yellow A (HSYA) may reduce ischemia/reperfusion (I/R) injury. However, the underlying molecular mechanisms remain unclear. The present study explored the effect and the mechanisms of HSYA on myocardial injury in vivo and in vitro. Myocardial infarct size was assessed by Evans blue/2,3,5?triphenyltetrazoliumchloride staining. Levels of cardiac troponin I (cTnI), interleukin?6 (IL?6), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured using commercial kits. Alteration of mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) generation was determined by fluorescent signals. Apoptosis was detected by terminal deoxynucleotidyl?transferase?mediated dUTP nick?end labeling staining, flow cytometry assay and caspase?3 activity. Expression levels of the apoptosis?associated proteins were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. In vivo, animals treated with HSYA presented less severe myocardial injury and decreased janus kinase 2 (JAK2)/signal transducer and activator of transcription 1 (STAT1) activity, improved antioxidant capacity and decreased apoptosis. In vitro, compared with the hypoxia (H)/reoxygenation (R) + HSYA group, AG490 and S1491 treatment decreased the releases of cTnI, IL?6 and LDH and enhanced the resistance to oxidative stress by maintaining MMP and decreasing ROS generation. In addition, AG490 and S1491 were also identified to alleviate the H/R?induced apoptosis by inhibiting caspase 3 activity and modulating the expression levels of cleaved caspase?3, tumor necrosis factor receptor superfamily member 6 (Fas), Fas ligand, B?cell lymphoma 2 (Bcl?2) and Bcl?2?associated X protein. These data suggested that inactivation of the JAK2/STAT1 pathway strengthened the HSYA?induced protective effect in H/R?induced myocardial injury. In conclusion, the treatment of HSYA was effective in decreasing IR?induced myocardial injury, and this may be largely dependent on the JAK2/STAT1 pathway. Therefore, the present study provided a potential strategy to prevent myocardial I/R injury.
Hydroxysafflor Yellow A mitigated myocardial ischemia/reperfusion injury by inhibiting the activation of the JAK2/STAT1 pathway.
Zhou D1, Ding T1, Ni B1, Jing Y1, Liu S1.
A simple, precise and reliable LC-MS/MS method was developed and validated for simultaneous quantification of vitexin, notoginsenoside R1, hydroxysafflor yellow A, ginsenoside Rd, puerarin, daidzein and senkyunolide I as components of Naodesheng (NDS) in rat serum. The Linearity ranges in rat serum were 0.045-4.5?μg/mL for vitexin, 0.0476-4.76?μg/mL for notoginsenoside R1, 0.0422-4.22?μg/mL for hydroxysafflor yellow A, 0.0426-4.26?μg/mL for ginsenoside Rd, 0.0436-4.36?μg/mL for puerarin, 0.026-2.6?μg/mL for daidzein, and 0.05-5?μg/mL for senkyunolide I, with the correlation coef?cients greater than 0.99. The established method was validated in terms of intra- and inter-day precision and accuracy, recovery, matrix effect and stability. Furthermore, the method was successfully applied for pharmacokinetic study of these seven components in rat serum after oral administration of NDS.
Copyright ? 2019 Elsevier B.V. All rights reserved.
LC-MS/MS; Naodesheng; Pharmacokinetic study; Simultaneous quantification of seven components
Validated LC-MS/MS method for simultaneous quantification of seven components of Naodesheng in rat serum after oral administration and its application to a pharmacokinetic study.
Luo L1, Kang J1, Zhao W1, Qi Y1, Liang S2.
2019 Sep 10;