RESUMO
Ischemic stroke is one of the leading causes of death and disability worldwide. In Han dynasty， HUA Tuo proposed the original preventive medicine idea that "with good blood circulation， the disease cannot be born"， which opened a broad space for the cross-research of blood-related mechanical factors and pharmacology. In the pathogenesis of ischemic stroke， mechanical factors comprehensively affect the function and crosstalk of platelets and endothelial cells. In recent years， as the well-known effects on thrombosis and stroke， more attention has been paid to hemodynamic factors as the participants involved in pathological mechanisms and potential therapeutic targets of ischemic stroke. The mechanical force ion channel Piezo1 widely exists on the surface of many types of cells. Besides being regulated by chemical and endogenous substances， Piezo1 responds to different mechanical conditions， regulates the opening and closing of channels， and activates different downstream signaling pathways. Piezo1 is now regarded as an important connection between mechanical and biochemical signals. A variety of Chinese medicine can affect the activity of Piezo1 protein， which may prevent and treat thrombotic diseases such as ischemic stroke through Piezo1 protein. In this paper， the effects of Piezo1 protein on the physiological and pathological functions of endothelial cells and platelet under different mechanical conditions and the role of Piezo1 in the process of thrombosis were reviewed， as well as the effects of Chinese medicine， chemical medicine， and endogenous substances targeting Piezo1 channel. These could provide new ideas for further exploring the mechanisms of Chinese medicines in activating blood circulation， developing new drugs， and deepening biomechanical-pharmacology research.
RESUMO
Objective To study effects of flow shear stress combined with salvianolic acid B (Sla B) on anti-platelet aggregation and its possible mechanism under the theoretical framework of biomechanopharmacology. Methods 2×4 factor experimental design was employed. By using Bioflux 1000 microfluidic system, shear stresses of 0.02 Pa and 1.5 Pa were applied together with four levels of Sla B concentration treatment on human vascular endothelial cells (HUVECs) for 20 hours. Then the cell supernatant was collected to detect concentration of 6-keto-PGF1α and vWF by ELISA and their effects on ADP-induced platelet aggregation were tested. Immunofluorescence method was used to detect vWF in endothelial cell cytoplasm. Results Physical shear stress of 1.5 Pa combined with Sla B of 100 μg/mL could significantly promote the endothelial secretion of 6-keto-PGF1α as compared to low shear stress condition (P<0.05). The endothelial cell supernatant under shear stress of 1.5 Pa showed an obvious anti-platelet aggregation effect. As the single factor, shear stresses significantly influenced vWF secretion (P<0.01), but Sla B had no obvious effects on vWF secretion. Conclusions Sla B inhibited ADP-induced platelet aggregation by increasing endothelial secretion of PGI2 under physical shear stresses. From the view of biomechaopharmacology (interaction between blood flow, blood vessel and blood), the physical flow shear stress is beneficial for the anti-thrombosis effect of Sla B.