Home General Physiology and Biophysics 2025 General Physiology and Biophysics Vol.44, No.1, p, 51–61, 2025

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Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
Published in English,
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General Physiology and Biophysics Vol.44, No.1, p, 51–61, 2025

Title: Senkyunolide A attenuates cerebral ischemia-reperfusion injury by inhibiting NLRP3-mediated ferroptosis in PC12 cells
Author: Qian Zhang, Yale Wang, Yihong Xiu, Zhiqiang Zhang, Tianyu Zou, Hongyan Wu, Yaping Quan

Abstract: Cerebral ischemia-reperfusion (I/R) is a serious complication in patients with ischemic stroke. Senkyunolide A (SenA) can alleviate neuronal cell damage induced by cerebral I/R; however, the exact action mechanism remains unclear. An in vitro cellular injury model was established by inducing PC-12 cells with OGD/R. The viability of SenA-treated PC-12 cells with or without OGD/R induction was detected with CCK-8 assay while the cell apoptosis was detected using TUNEL. The secretion of inflammatory cytokines, the activity of ROS, mitochondrial membrane potential and mtROS level were measured with ELISA, ROS assay kits, JC-1 staining and MitoSOX Red assay, respectively. The level of Fe2+ was detected with Fe2+ assay kits and lipid peroxidation was detected with TBARS assay. The expressions of lipid peroxides were measured using corresponding assay kits. Western blot was used to measure the expressions of NLRP3, apoptosis-, and ferroptosis-related proteins. The transfection efficiency of OV-NLRP3 was also detected using Western blot. The present study showed that SenA could attenuate viability damage, inflammatory response, oxidative stress, apoptosis and ferroptosis in OGD/R-induced PC-12 cells and it was identified that the cytoprotective effects of SenA on PC-12 cells stimulated by OGD/R may be associated with the inhibition of NLPR3. Collectively, SenA protects neuronal cells against cerebral I/R injury through the inhibition of NLRP3-mediated ferroptosis.

Keywords: Cerebral ischemia-reperfusion — Senkyunolide A — NLPR3 — Ferroptosis
Year: 2025, Volume: 44, Issue: 1 Page From: 51, Page To: 61
doi:10.4149/gpb_2024038


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