Hydroxysafflor yellow A and anhydrosafflor yellow B alleviate ferroptosis and parthanatos in PC12 cells injured by OGD/R

2021 ◽  
Author(s):  
Guangwei Chen ◽  
Chang Li ◽  
Ling Zhang ◽  
Jiehong Yang ◽  
Huanhuan Meng ◽  
...  
Keyword(s):  
Hydroxysafflor Yellow A

Hydroxysafflor Yellow A Attenuates Renal Ischemia- Reperfusion Injury in a Rat Model

2012 ◽  
Vol 9 (10) ◽  
pp. 967-972
Author(s):  
Weiran Chai ◽  
Wenhui Zhang ◽  
Zhu Jin ◽  
Yanqian Zheng ◽  
Peiyao Jin ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Hydroxysafflor Yellow A ◽  
Renal Ischemia Reperfusion Injury

Hydroxysafflor yellow A inhibits IL-1β-induced release of IL-6, IL-8, and MMP-1 via suppression of ERK, NF-κB and AP-1 signaling in SW982 human synovial cells

2016 ◽  
Vol 7 (11) ◽  
pp. 4516-4522 ◽  
Author(s):  
Bin-Feng Cheng ◽  
Yao-Xin Gao ◽  
Jun-Jiang Lian ◽  
Dan-Dan Guo ◽  
Lei Wang ◽  
...  
Keyword(s):  
Synovial Cells ◽  
Hydroxysafflor Yellow A

Hydroxysafflor yellow A reduces IL-6, IL-8, and MMP-1 release via inhibiting ERK, NF-κB and AP-1 signaling in SW982 cells.

Hydroxysafflor yellow A promotes angiogenesis in rat brain microvascular endothelial cells injured by oxygen-glucose deprivation/reoxygenation(OGD/R) through SIRT1-HIF-1α-VEGFA signaling pathway

2021 ◽  
Vol 18 ◽  
Author(s):  
Juxuan Ruan ◽  
Lei Wang ◽  
Jiheng Dai ◽  
Jing Li ◽  
Ning Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Ischemia Reperfusion ◽  
Tube Formation ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Hydroxysafflor Yellow A ◽  
Microvascular Endothelial

Objective: Angiogenesis led by brain microvascular endothelial cells (BMECs) contributes to the remission of brain injury after brain ischemia reperfusion. In this study, we investigated the effects of hydroxysafflor yellow A(HSYA) on angiogenesis of BMECs injured by OGD/R via SIRT1-HIF-1α-VEGFA signaling pathway. Methods: The OGD/R model of BMECs was established in vitro by OGD for 2h and reoxygenation for 24h. At first, the concentrations of vascular endothelial growth factor (VEGF), Angiopoietin (ang) and platelet-derived growth factor (PDGF) in supernatant were detected by ELISA, and the proteins expression of VEGFA, Ang-2 and PDGFB in BMECs were tested by western blot; the proliferation, adhesion, migration (scratch healing and transwell) and tube formation experiment of BMECs; the expression of CD31 and CD34 were tested by immunofluorescence staining. The levels of sirtuin1(SIRT1), hypoxia-inducible factor-1α (HIF-1α), VEGFA mRNA and protein were tested. Results: HSYA up-regulated the levels of VEGF, Ang and PDGF in the supernatant of BMECs under OGD/R, and the protein expression of VEGFA, Ang-2 and PDGFB were increased; HSYA could significantly alleviate the decrease of cell proliferation, adhesion, migration and tube formation ability of BMECs during OGD/R; HSYA enhanced the fluorescence intensity of CD31 and CD34 of BMECs during OGD/R; HSYA remarkably up-regulated the expression of SIRT1, HIF-1α, VEGFA mRNA and protein after OGD/R, and these increase decreased after SIRT1 was inhibited. Conclusion: SIRT1-HIF-1α-VEGFA signaling pathway is involved in HSYA improves angiogenesis of BMECs injured by OGD/R.

The Effects and Mechanisms of Improvement of Hydroxysafflor Yellow A in Pulmonary Fibrosis

2022 ◽  
Vol 12 (4) ◽  
pp. 834-840
Author(s):  
Peng Xu ◽  
Fang Sun ◽  
Ming Xiong ◽  
Qun Li ◽  
Peng Tu ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Sham Group ◽  
Model Group ◽  
Hydroxysafflor Yellow A ◽  
Masson Staining ◽  
E Cadherin

Purpose: To discuss the effects and mechanisms of improvement of Hydroxysafflor yellow A in pulmonary fibrosis by in vivo study. Material and Methods: In this study, dividing the C57BL/6 mice as 4 group, there were 10 mice in every group. Collecting the serum of difference groups and measuring the Hyp, SOD, MDA, TNF-α and IL-6 levels. Lung tissues were taken out and evaluating the pathology by HE staining and fibrosis degree by Masson staining. The relative proteins (α-SMA and E-cadherin) were measured by IHC and WB in lung tissues of difference groups. Results: With HSYA or DXM supplement, the Hyp, MDA, TNF-α and IL-6 concentrations significantly suppressed and SOD concentration significantly enhanced (P < 0.05, respectively). Compared with Sham group, the pathology injury and fibrosis degree of Model group were significantly up-regulation (P < 0.001, respectively); With HSYA or DXM treatment, the pathology injury and fibrosis degree of HSYA and DXM groups were significantly improved (P < 0.05, respectively). By IHC and WB assay, the α-SMA and E-cadherin proteins expressions of Model group were significantly differences (P < 0.001, respectively); however, the α-SMA and E-cadherin proteins expressions of HSYA and DXM groups were significantly improved with HSYA or DXM supplement (P < 0.05, respectively). Conclusion: HSYA improves pulmonary fibrosis by regulation α-SMA and E-cadherin in vivo study.

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