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Hydroxysafflor yellow a attenuates oxygen-glucose deprivation/ reoxygenation induced endothelial pyroptosis via PARP-1/NLRP3 pathway.

Overview

Authors: Qingxia Huang1, Shennan Shi1, Lizhi Qian1, Yanqing Wu1, Bingyan Mao1, Nipi Chen1, Chaodong Qian1, Yan Guo2, Bo Jin1
  1. School of Life Sciences, Zhejiang Chinese Medical University, Hangzhou, China
  2. School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Hangzhou, China
Institutions: Zhejiang Chinese Medical University (China)
Journal: Frontiers in pharmacology, volume 17, article 1811680
Dates: received 15 February 2026; accepted 4 May 2026; published online 21 May 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.3389/fphar.2026.1811680 · PMID 42256403 · PMCID PMC13233435 · OpenAlex W7161975176
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: cellular / molecular (subfield)
Methods: Statistics
Keywords: HSYA, NLRP3, PARP-1, pyroptosis, rBMECs
Topic: Sunflower and Safflower Cultivation (Plant Science, Agricultural and Biological Sciences), according to OpenAlex
Funding: National Natural Science Foundation of China (82374071, LY23H280006)
Citations: not cited yet (Europe PMC); 24 references in the paper

Abstract

Introduction: Dysfunction of brain microvascular endothelial cells (BMECs) induced by oxidative stress represents a critical event in the pathogenesis of ischemia/reperfusion (I/R) injury. Although previous investigations have demonstrated the protective effects of Hydroxysafflor yellow A (HSYA) against I/R injury, the precise underlying mechanisms remain incompletely understood.

Methods: An oxygen-glucose deprivation/reoxygenation (OGD/R) model was established in rat BMECs (rBMECs). We analyzed cell viability, proliferation, oxidative stress markers (SOD, JC-1), and pyroptosis-related protein expression (NLRP3, Caspase-1, GSDMD, IL-1β). The NLRP3 inhibitor MCC950 was utilized to elucidate HSYA’s regulatory role in OGD/R-induced pyroptosis. The network pharmacology approach was used to identify potential targets of HSYA against ischemia/reperfusion (I/R) injury. Molecular docking, molecular dynamics (MD) simulation, CETSA, DARTS assays, along with PARP-1 overexpression/inhibition experiments were performed to elucidate the underlying mechanism of HSYA in ameliorating I/R injury.

Results: The results indicated that HSYA enhanced cell viability and proliferation of rBMECs exposed to OGD/R injury, accompanied by increased SOD activity and preserved MMP. HSYA suppressed the expression of pyroptosis-related proteins (NLRP3, Caspase-1, GSDMD, and IL-1β). The protective effects of HSYA were comparable to those observed with the NLRP3 inhibitor MCC950. Cotreatment afforded superior protection and more pronounced inhibition of NLRP3-mediated pyroptosis in OGD/R-induced rBMECs. Network pharmacology identified PARP-1 as a key target of HSYA against I/R injury. This interaction was validated through molecular docking and MD simulation, which revealed stable binding with high-affinity. Further experimental validation using CETSA and DARTS assays confirmed the direct binding of HSYA to PARP-1. Modulation of PARP-1 activity resulted in altered NLRP3 expression; Notably, both the PARP-1 inhibitor Olaparib and HSYA suppressed NLRP3, suggesting that the protective effects of HSYA may be attributed to direct targeting of PARP-1/NLRP3 pathway.

Discussion: This study demonstrates that HSYA protects rBMECs against OGD/R injury by directly targeting PARP-1, thereby inhibiting the NLRP3-mediated pyroptosis pathway. These findings reveal a novel mechanism of HSYA in mitigating I/R injury and implicate PARP-1 as a promising therapeutic target. Nevertheless, several limitations should be considered. The precise molecular details between PARP-1 and the NLRP3 inflammasome pathway require further elucidation, and our findings remain to be validated using animal models of cerebral I/R injury.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

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Data

Datasets cited

Other data links

  • ncbi.nlm.nih.gov/geo, NCBI; found in the text, “Identification of HSYA-I/R injury targets and…”

Data availability statement

The datasets presented in this study can be found in online repositories. The names of the repository/repositories and accession number(s) can be found in the article/Supplementary Material.

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 2, 28 September 2026

  • Funding: added National Natural Science Foundation of China: 82374071, LY23H280006

Version 1, 28 September 2026: the first record

Recorded: type, language, journal, volume, pages, dates, 9 authors, 5 keywords, 24 references.

Cite

This paper

Huang, Q., Shi, S., Qian, L., Wu, Y., Mao, B., Chen, N., Qian, C., Guo, Y., & Jin, B. (2026). Hydroxysafflor yellow a attenuates oxygen-glucose deprivation/ reoxygenation induced endothelial pyroptosis via PARP-1/NLRP3 pathway. Frontiers in pharmacology, 17, 1811680. https://doi.org/10.3389/fphar.2026.1811680

BibTeX

@article{huang2026hydroxysafflor,
author = {Huang, Qingxia and Shi, Shennan and Qian, Lizhi and Wu, Yanqing and Mao, Bingyan and Chen, Nipi and Qian, Chaodong and Guo, Yan and Jin, Bo},
title = {{Hydroxysafflor yellow a attenuates oxygen-glucose deprivation/ reoxygenation induced endothelial pyroptosis via PARP-1/NLRP3 pathway}},
journal = {Frontiers in pharmacology},
year = {2026},
month = may,
volume = {17},
pages = {1811680},
publisher = {Frontiers Media SA},
issn = {1663-9812},
doi = {10.3389/fphar.2026.1811680},
url = {https://doi.org/10.3389/fphar.2026.1811680},
pmid = {42256403},
pmcid = {PMC13233435}
}

RIS

TY - JOUR
AU - Huang, Qingxia
AU - Shi, Shennan
AU - Qian, Lizhi
AU - Wu, Yanqing
AU - Mao, Bingyan
AU - Chen, Nipi
AU - Qian, Chaodong
AU - Guo, Yan
AU - Jin, Bo
TI - Hydroxysafflor yellow a attenuates oxygen-glucose deprivation/ reoxygenation induced endothelial pyroptosis via PARP-1/NLRP3 pathway
T2 - Frontiers in pharmacology
J2 - Front Pharmacol
PY - 2026
DA - 2026/05/21
VL - 17
SP - 1811680
SN - 1663-9812
PB - Frontiers Media SA
DO - 10.3389/fphar.2026.1811680
UR - https://doi.org/10.3389/fphar.2026.1811680
LA - en
ER -

CSL-JSON

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