Tetramethylpyrazine Inhibits Platelet Adhesion and Inflammatory Response in Vascular Endothelial Cells by Inhibiting P38 MAPK and NF-κB Signaling Pathways

Damaged vascular endothelial cells after ischemic stroke release inflammatory cytokines and adhesion molecules, which could trigger platelet adhesion to vascular endothelial cells and platelet activation, and accelerate thrombus formation. Tetramethylpyrazine is the main bioactive component of Chuanxiong, which has demonstrated considerable protective effects in cerebrovascular diseases. However, the effect and mechanisms of tetramethylpyrazine on platelet adhesion to ischemia/reperfusion-injured endothelial cells have not been elucidated. In this study, we established an oxygen-glucose deprivation/reoxygenation (OGD/R)-induced brain microvascular endothelial cells (BMECs) injury model to investigate the protective effects of tetramethylpyrazine on platelet adhesion to endothelial cells and potential mechanisms. Experimental results showed that tetramethylpyrazine inhibited platelets adhesion to BMECs, alleviated expression of inflammatory cytokines and adhesion molecules on BMECs, and protected BMECs injured by OGD/R. Furthermore, tetramethylpyrazine could inhibit P38 MAPK and NF-kappa B activation in injured BMECs by OGD/R and inhibition of P38 MAPK with SB303580 and NF-kappa B with Bay-11-7082 attenuated the reduction of platelets adhesion to BMECs by tetramethylpyrazine. In conclusion, tetramethylpyrazine protected BMECs and inhibited platelets adhesion to BMECs after OGD/R injury, which was partially mediated by inhibiting P38 MAPK and NF-kappa B signaling pathways.