Neuroprotective effects of SOX5 against ischemic stroke by regulating VEGF/PI3K/AKT pathway

Ischemic stroke is a common clinical cardiovascular disease and often accompanied by central nervous system injury. It often causes paralysis or loss of motor function after central nervous system injury and significantly reduces the patient's quality of life. At present, there is no effective treatment strategy for nerve damage caused by ischemic stroke. Therefore, it is urgently need to explore effective treatment targets. The protein expression of SOX5, VEGF and apoptosis related proteins were measured by western blot. The mRNA expression of SOX5 and VEGF were detected by RT-qPCR. The concentration of S100B and GFAP which are related to nerve damage were detected using ELISA assay. The transcriptional regulation of SOX5 on VEGF was detected using ChIP-PCR and dual luciferase reporter gene assays. The cell apoptosis was measured by TUNEL assay and cell viability was detected by CCK-8 assay. In our study, we found that the expression of SOX5 was significantly reduced when LPS induced apoptosis in PC-12 cells. Overexpression of SOX5 repaired LPS-induced apoptosis. SOX5 promotes VEGF expression as a transcription factor to activate the PI3K/AKT pathway. VEGF also repairs nerve injury and brain tissue injury caused by ischemic stroke. In conclusion, SOX5 transcription regulates the expression of VEGF to activate the PI3K/AKT pathway, which repaired nerve damage caused by ischemic stroke. Therefore, SOX5 could be a new target to regulate VEGF which can repair nerve injury induced by ischemic stroke.

Automated summary

Ischemic stroke-induced nerve damage significantly impacts patients' quality of life, necessitating the search for effective treatments. Research has shown that SOX5 transcription regulates VEGF expression and activates the PI3K/AKT pathway to repair nerve damage.