Hydroxysafflor yellow A (HSYA) is a flavonoid derived and isolated from traditional Chinese medicine Carthamus tinctorius L., possessing anti-tumor activity. It can suppress foam cell formation, vascular endothelial cell dysfunction, vascular smooth muscle cell proliferation and migration, and platelet activation. Besides, HSYA is devoted to lowering blood lipids, regulating ion channels, reducing vascular inflammation, and protecting pancreatic beta cells[3]. HYSA could inhibit LPS-induced VSMCs proliferation and migration, accompanied by the downregulated levels of several key pro-inflammatory cytokines, including TNF-α, IL-6, and IL-8. HYSA inhibited LPS-induced upregulation of TLR-4 expression as well as the activation of Rac1/Akt pathway[4]. HSYA (14, 28, 56 mg/kg, i.p.) has a protective effect on acute respiratory distress syndrome (ARDS) induced by LPS through blocking the TLR4/NF-κB pathway, and that the TLR4 receptor might be a target of HSYA on the cell membrane[5]. 8 mg/kg and 16 mg/kg HSYA administration by common carotid artery (CCA) injection improved impaired cognitive function in Morris water maze (MWM) and passive avoidance tasks. And 8 mg/kg HSYA treatment rescued the impaired long-term potentiation (LTP) in hippocampus of MCAO (middle cerebral artery occlusion) rats[6].
Hydroxysafflor yellow A/羟基红花黄色素A 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Rat aortic endothelial cells (RAECs)
7.5 μmol/L
24 and 48 hours
To evaluate the effects of hydroxysafflor yellow A on the production of coagulation-associated factors by LPS-stimulated endothelial cells. Results showed that hydroxysafflor yellow A significantly reduced the production of sTM and TF and increased the production of TFPI.
Acta Pharmacol Sin. 2024 May;45(5):1077-1092
Rat peritoneal macrophages
7.5 μmol/L
24 and 48 hours
To evaluate the effects of hydroxysafflor yellow A on the production of pro-inflammatory cytokines by LPS-stimulated macrophages. Results showed that hydroxysafflor yellow A significantly inhibited the production of TNF-α, IL-6, IL-1β, and HMGB1.
Acta Pharmacol Sin. 2024 May;45(5):1077-1092
Rat splenic regulatory T cells (Tregs)
7.5 μmol/L
72 hours
To evaluate the effects of hydroxysafflor yellow A on the function and apoptosis of LPS-stimulated Tregs. Results showed that hydroxysafflor yellow A significantly reduced the expression levels of CTLA-4 and FOXP3, decreased IL-10 secretion, and increased the apoptosis rate of Tregs.
Acta Pharmacol Sin. 2024 May;45(5):1077-1092
Co-culture of human endometrial perivascular stem cells (En-PSCs) with HUVECs
50 μM HSYA
3 hours
Assess synergistic effects of En-PSCs/HSYA on angiogenesis, demonstrating enhanced tube formation and branching points.
Stem Cell Res Ther. 2024 Jul 18;15(1):217
Human umbilical vein endothelial cells (HUVECs)
50 μM
3 hours
Evaluate the effect of HSYA on angiogenesis in HUVECs, showing significantly increased tube formation.
Stem Cell Res Ther. 2024 Jul 18;15(1):217
Hydroxysafflor yellow A/羟基红花黄色素A 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Sprague-Dawley rats
Cecal ligation and puncture (CLP)-induced sepsis model
Intravenous injection
4 mL/kg
Administered at 2, 12, 24, 36, 48, and 60 h after surgery, for 7 days
To evaluate the effects of hydroxysafflor yellow A on immune regulation, inflammation inhibition, coagulation modulation, and protection against multiple organ dysfunction in CLP rats. Results showed that hydroxysafflor yellow A significantly reduced the expression levels of CTLA-4 and FOXP3, decreased IL-10 secretion, increased the apoptosis rate of Tregs, inhibited the production of pro-inflammatory cytokines, modulated coagulation status, and improved multiple organ function. Additionally, hydroxysafflor yellow A significantly increased the survival rate of CLP rats.
Acta Pharmacol Sin. 2024 May;45(5):1077-1092
Sprague-Dawley rats
Spinal cord compression injury model
Intraperitoneal injection
8 mg/kg (at 1 and 6 h after injury), then 14 mg/kg for 7 days
Once at 1 and 6 h after injury, then once daily for 7 days
HSYA treatment significantly reduced tissue injury, oxidative stress, inflammatory response, and neuronal apoptosis, and improved limb functional recovery after spinal cord injury.
J Neuroinflammation. 2017 May 3;14(1):97
Zebrafish
TPEN-induced hematopoietic defect model
Aqueous solution immersion
100 μg/mL
Single treatment, lasting 12 hours
To evaluate the protective effects of HSYA on TPEN-induced hematopoietic defects in zebrafish. Results showed that HSYA significantly restored the number of HSCs and inhibited the P53 signaling pathway and oxidative stress.
MedComm (2020). 2023 Aug 24;4(5):e352
Mice
Oleic acid-induced acute lung injury model
15 mg/kg
Activation of anti-oxidant enzymes and inactivation of the inflammatory response via the cAMP/PKA pathway
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