ArticleFrontiers in pharmacology2026
Hydroxysafflor yellow a attenuates oxygen-glucose deprivation/ reoxygenation induced endothelial pyroptosis via PARP-1/NLRP3 pathway.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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