ArticleCells2022
Hydroxysafflor Yellow A Exerts Neuroprotective Effects via HIF-1α/BNIP3 Pathway to Activate Neuronal Autophagy after OGD/R.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Emerging natural product development strategies drive the therapeutic potential exploration and clinical translation of hydroxysafflor yellow A.Journal of pharmaceutical analysis · 2026Review
- Hydroxysafflor Yellow A improves diabetic nephropathy by inhibiting PI3K/AKT/mTOR pathway based on a multidimensional study.Frontiers in medicine · 2026Article
- A Novel Weight Loss Mechanism of Hydroxysafflor Yellow A in Obese Mice: Involvement of Immune Inflammation via Prkcd, Btk, and Vav1 Genes in Adipose Tissue.Current pharmaceutical biotechnology · 2026Article
- Neuroprotective potential of indian herbs in ischaemic stroke: a comprehensive review of pharmacological insights, therapeutic gaps, and future directions.Inflammopharmacology · 2025Review
- The geroprotective potential of chalcones.Nature communications · 2025Review
- Discovery of platelet glycoprotein VI receptor antagonists and their neuroprotective activity: an in silico, in vitro, and in vivo study.3 Biotech · 2025Article
- Hydroxysafflower yellow A alleviates the inflammatory response in astrocytes following cerebral ischemia by inhibiting the LCN2/STAT3 feedback loop.Metabolic brain disease · 2025Article
- Hydroxysafflor Yellow A Reduced Neuroinflammation Induced by Astrocyte-Derived IL-17A by Inhibiting the IL-17RA/ACT1/NF-κB/IL-17A Loop After OGD/R.Journal of inflammation research · 2025Article
- Inflammation-related biomarkers and berberine therapy in post-stroke depression: evidence from bioinformatics, machine learning, and experimental validation.Frontiers in neuroscience · 2025Article
- Article
- [Expression and significance of hypoxia-inducible factor 1α and Bcl-2/adenovirus E1B19kDa-interacting protein 3 in children with traumatic brain injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- Review
- Insight into interplay between PANoptosis and autophagy: novel therapeutics in ischemic stroke.Frontiers in molecular neuroscience · 2024Review
- A comprehensive review of stroke-related signaling pathways and treatment in western medicine and traditional Chinese medicine.Frontiers in neuroscience · 2023Review
- [Activation of the CaMKKβ/AMPK/HIF-1α signaling pathway promotes angiogenesis in endometriosis by regulating mitophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical UniversityArticle
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
In the process of ischemic stroke (IS), cellular macroautophagy/autophagy and apoptosis play a vital role in neuroprotection against it. Therefore, regulating their balance is a potential therapeutic strategy. It has been proved that hydroxysafflor yellow A (HSYA) has anti-inflammatory and antioxidant effects, which can both protect neurons. By exploring bioinformatics combined with network pharmacology, we found that HIF1A and CASP3, key factors regulating autophagy and apoptosis, may be important targets of HSYA for neuroprotection in an oxygen glucose deprivation and reperfusion (OGD/R) model. In this study, we explored a possible new mechanism of HSYA neuroprotection in the OGD/R model. The results showed that OGD/R increased the expression of HIF1A and CASP3 in SH-SY5Y cells and induced autophagy and apoptosis, while HSYA intervention further promoted the expression of HIF1A and inhibited the level of CASP3, accompanied by an increase in autophagy and a decrease in apoptosis in SH-SY5Y cells. The inhibition of HIF1A diminished the activation of autophagy induced with HSYA, while the inhibition of autophagy increased cell apoptosis and blocked the neuroprotective effect of HSYA, suggesting that the neuroprotective effect of HSYA should be mediated by activating the HIF1A/BNIP3 signaling pathway to induce autophagy. These results demonstrate that HSYA may be a promising agent for treating IS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.