The International journal of neuroscience · 2026
Liproxstatin-1 ameliorates cerebral ischemia-reperfusion injury through inhibiting ferroptosis.
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Xiong Lie, Jin Yuting, Zhang Jingruo, Shi Hanqiang, Zhu Gaofeng, Zhu Ping, Liu Yanlin, Luo Kaitao
Аннотация
OBJECTIVE: This study intends to investigate the protective impact of liproxstatin-1 against cerebral ischemia-reperfusion injury (CIRI) in rats and the corresponding underlying mechanism.
METHODS: CIRI rat models were constructed. Pathological changes in tissues were assessed at multiple levels, including infarct area, neuronal activity, and iron content through 2,3,5-triphenyl tetrazolium chloride (TTC) staining, Nissl staining and Prussian blue (PB) staining. The expression of oxidative damage factors and key ferroptosis-related genes was assessed by enzyme-linked immunosorbent assay (ELISA), quantitative real-time PCR (qPCR) or western blot (WB). Rat brain tissues were subjected to bulk RNA sequencing (bulk RNA-seq) analysis. Finally, in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) models were established, and the inhibitory effect of liproxstatin-1 on ferroptosis was identified by measuring cell viability, Fe2+ levels and lipid peroxidation.
RESULTS: In vivo experiments demonstrated that liproxstatin-1 markedly improved neurological function and neuronal pathological damage in CIRI rats, while reducing iron content and oxidative damage. Bulk RNA-seq analysis revealed that differentially expressed genes (DEGs) were mainly enriched in the IL-17 signaling pathway, ether lipid metabolism, TNF signaling pathway and ferroptosis. Consistently, qPCR and WB results showed that liproxstatin-1 treatment increased the expression of FTH1 and GPX4, while decreasing the expression of NOX1, ACSL4, COX2 and TFR1 in rat brain tissues. In vitro experiments further demonstrated that liproxstatin-1 significantly enhanced cell viability and reduced Fe2+ and reactive oxygen species (ROS) levels.
CONCLUSIONS: Liproxstatin-1 inhibits the process of ferroptosis and alleviates CIRI in rats.
METHODS: CIRI rat models were constructed. Pathological changes in tissues were assessed at multiple levels, including infarct area, neuronal activity, and iron content through 2,3,5-triphenyl tetrazolium chloride (TTC) staining, Nissl staining and Prussian blue (PB) staining. The expression of oxidative damage factors and key ferroptosis-related genes was assessed by enzyme-linked immunosorbent assay (ELISA), quantitative real-time PCR (qPCR) or western blot (WB). Rat brain tissues were subjected to bulk RNA sequencing (bulk RNA-seq) analysis. Finally, in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) models were established, and the inhibitory effect of liproxstatin-1 on ferroptosis was identified by measuring cell viability, Fe2+ levels and lipid peroxidation.
RESULTS: In vivo experiments demonstrated that liproxstatin-1 markedly improved neurological function and neuronal pathological damage in CIRI rats, while reducing iron content and oxidative damage. Bulk RNA-seq analysis revealed that differentially expressed genes (DEGs) were mainly enriched in the IL-17 signaling pathway, ether lipid metabolism, TNF signaling pathway and ferroptosis. Consistently, qPCR and WB results showed that liproxstatin-1 treatment increased the expression of FTH1 and GPX4, while decreasing the expression of NOX1, ACSL4, COX2 and TFR1 in rat brain tissues. In vitro experiments further demonstrated that liproxstatin-1 significantly enhanced cell viability and reduced Fe2+ and reactive oxygen species (ROS) levels.
CONCLUSIONS: Liproxstatin-1 inhibits the process of ferroptosis and alleviates CIRI in rats.