Butylphthalide

Acute cerebral infarction profoundly affects patients' neurological function and quality of life. This study explores the impact of Solitaire AB stent thrombectomy, combined with tirofiban and butylphthalide, on neurological function and inflammatory factors in patients with acute cerebral infarction.

Seventy-three eligible patients treated between 2021 and 2023 were divided into a control group (Solitaire AB stent thrombectomy) and a treatment group (Solitaire AB stent thrombectomy with tirofiban and butylphthalide). Postoperative neurological function scores and inflammatory factor levels were analyzed.

The treatment group demonstrated a higher clinical effective rate, lower National Institutes of Health Stroke Scale scores at one day and seven days and higher Mini-Mental State Examination and Montreal Cognitive Assessment scores post-treatment. Inflammatory factor levels (Neuron Specific Enolase (NSE), S100-β, TNF-α and IL-6) were lower in the treatment group. No significant differences in adverse outcomes were observed.

Solitaire AB stent thrombectomy with tirofiban and butylphthalide shows superior efficacy, improving neurological function and inflammatory factors without increasing adverse outcomes. This offers valuable insights for clinical treatment of acute cerebral infarction.

Acute cerebral infarction (CI) is characterized by acute onset, high disability rate, and high morbidity rate, which seriously threatens the health and safety of people and places a heavy burden on individuals and the country. This study aimed to explore the effects of butylphthalide on nerve cell ferroptosis in CI rats and its underlying mechanisms. Middle cerebral artery occlusion (MCAO) rat model was used to study the effect of butylphthalide on acute CI in vivo and oxygen glucose deprivation (OGD) model was used to study the effect of butylphthalide on acute CI in vitro. Our findings demonstrated that butylphthalide markedly reduced oxidative damage and ferroptosis in the brains of MCAO rats. Furthermore, we found that butylphthalide upregulated the netrin-1/deleted in colorectal cancer (DCC)/vascular endothelial growth factor (VEGF) signaling axis, which regulates NF-E2-related factor-2 (NRF2) expression and contributes to ferroptosis in the MCAO rat model and OGD-treated HT22 cells. Collectively, our findings indicate that butylphthalide inhibits oxidative stress-mediated ferroptosis in the MCAO rat model and OGD-treated HT22 cells by modulating the netrin-1/DCC/VEGF/NRF2 axis. In conclusion, our results reveal a novel mechanism for the protection of acute CIs by butylphthalide.