A Preliminary Study On The Relationship Between Thromboxane A2 Receptor And Ischemic Cerebral Infarction

Background and purpose: Cerebral infarction is of great concern because of its high incidence,high disability and high mortality.Research on the pathogenesis and treatment of cerebral infarction has always been a hot spot in the medical field.Thromboxane A2 receptor(TXA2R)is a widely distributed coagulation and inflammation-related receptor in human body and is thought to have a strong association with cerebral infarction.Studies have shown that the gene polymorphism of TXA2 R rs768963 in the population affects the incidence of cerebral infarction,while the use of TXA2 R antagonist SQ29548 can inhibit the degree of brain injury after cerebral infarction in animal models.They may be related to the role of TXA2 R in platelet activation and neuronal injury following cerebral infarction,but the specific mechanisms are not yet clear.Therefore,we hope to explore the role of rs768963 mutation in the pathogenesis of cerebral infarction and post-cerebral infarction TXA2 R and nerve cell damage between the specific mechanism of action,which will provide new clues for the onset and treatment of cerebral infarction.Materials and Methods: The platelet function of the subjects was detected using the platelet aggregation rate and PMA level.The relationship between rs768963 mutation and platelet function was analyzed by PCR-LDR identify the rs768963 genotype of the subject.SH-SY5 Y cells were used as neuronal cell model in vitro and treated with TXA2R-specific antagonist SQ29548 for H2O2 stimulation.The neuronal survival,oxidative stress response,apoptosis and activation of related pathways were measured by WST-1,LDH,immunofluorescence,flow cytometry and Western blot.Results: Mutation of rs768963 on the TXA2 R gene affects the maximum platelet aggregation rate induced by arachidonic acid in patients with cerebral infarction without antiplatelet agents.The TXA2R-specific antagonist SQ29548 can improve the survival and viability of SH-SY5 Y cells under H2O2 action,reduce the oxidative stress and apoptosis level,and protect the neurons.Conclusion: TXA2 R gene mutation can affect patients with cerebral infarction platelet function.The use of TXA2 R antagonists can reduce the oxidative stress response of nerve cells to protect the role of nerve cells.