The upregulation of caveolin-1 expression via the TLR4-Myd88 pathway contributes to cerebral vasospasm.

Cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH) significantly impacts patient morbidity and mortality. This study aimed to investigate the role of the TLR4-MyD88 signaling pathway in the pathogenesis of CVS and its relationship with Caveolin-1 (CAV-1). We established a rat model of SAH using the double blood injection method in the cisterna magna to induce CVS. Various techniques, including pathological assessments, immunohistochemistry, Western blotting, and RT-qPCR, were employed to evaluate the expression of Toll-like receptor 4 (TLR4), MyD88, NF-κB, and CAV-1. The results showed a significant upregulation of TLR4, MyD88, NF-κB, and CAV-1 in SAH rats, with the upregulation correlating with CVS. Furthermore, the application of methyl-β-cyclodextrin (MβCD) effectively reduced CAV-1 expression and ameliorated CVS severity. Additionally, dexmedetomidine (DEX) treatment downregulated inflammatory markers and improved CVS, suggesting a potential therapeutic role through modulating the TLR4-MyD88 pathway. This study highlights the complex interplay between neuroinflammation, CAV-1, and CVS, proposing new avenues for therapeutic interventions in managing CVS post-SAH.