Compound A9抑制蛛网膜下腔出血后谷氨酸诱导神经细胞铁死亡的研究OA

Objective To investigate whether glutamate induces ferroptosis in neurons following subarachnoid hemorrhage(SAH)and to explore the neuroprotective effect of Compound A9.Methods Eighty Sprague-Dawley rats were randomly divided into four cohorts:a sham-operated control group,an SAH model group,an SAH model+glutamate group,and an SAH model+glutamate+Compound A9 group.At 48 hours post-SAH,neurological function was assessed using a standardized scoring system,while the lev-els of glutathione(GSH)and lactate dehydrogenase(LDH)were quantified via enzyme-linked immunosorbent assay(ELISA).Western blot analysis was employed to determine the expression levels of 4-hydroxynonenal(4-HNE)and glutathione peroxidase 4(GPX4),and immunofluorescence staining was conducted to colocalize 4-HNE with Neun,a neuronal marker.Foot fault tests were performed on days 5,7,and 12 to evaluate motor coordination.Results Compound A9 mitigated glutamate-induced neurological deficits and motor function impairments post-SAH.It also reduced oxidative damage and lipid peroxidation induced by glutamate.Furthermore,Compound A9 suppressed glutamate-induced ferroptosis by upregulating GPX4 expression.Conclusion Glutamate induces ferropto-sis in neurons following SAH,and Compound A9 inhibits glutamate-induced ferroptosis by upregulating GPX4 expression.