Carthamin yellow (CY), a flavonoid compound extracted from safflower, has been reported to attenuate cardiac ischemia and reperfusion injury. However, whether CY could ameliorate ischemic stroke is not completely understood. In the present study, the preventive effects of CY on experimental ischemic stroke were investigated using middle cerebral artery occlusion (MCAO) model rats. Neurological scores, brain edema, infarct area and microtubule‑associated protein 2 (MAP‑2) immunoreactivity were assessed to evaluate the effects of CY on ischemic brain injury. The involvement of inflammation and ferroptosis were examined to investigate the mechanism underlying the effects of CY. The results demonstrated that 2‑week CY treatment attenuated the neurological deficit score, brain water content and infarct area, and increased MAP‑2 immunoreactivity in the cortex in MCAO model rats. CY administration also deactivated the cortex NF‑κB/NLR family pyrin domain containing 3 inflammasome signaling pathway, and decreased serum TNF‑α, IL‑1β and IL‑6 concentrations. Moreover, CY treatment inhibited Fe2+ and reactive oxygen species accumulation, and reversed acyl‑CoA synthetase long‑chain family member 4, transferrin receptor 1, glutathione peroxidase 4 and ferritin heavy chain 1 protein expression levels in the brain. The levels of glutathione, superoxide dismutase and malondialdehyde in the serum were also reversed by CY treatment. Collectively, the results of the present study demonstrated that CY protected rats against ischemic stroke, which was associated with mitigation of inflammation and ferroptosis.
Keywords: ischemic stroke; carthamin yellow; microtubule‑associated protein 2; ferroptosis; NF‑κB/NLRP3 inflammasome.