血管内皮细胞凋亡导致的有效循环血容量骤减是烧伤休克发生的病生基础，目前尚无有效保护方案，休克仍是烧伤救治的重点和难点。课题组前期的研究发现，烧伤休克血清下调的miR-4793-3p可靶向调控hMSC生成VEGF，发挥抑制血管内皮细胞凋亡的作用，但具体机制尚不清楚。据此提出，miR-4793-3p调控hMSC生成和旁分泌VEGF，通过激活PI3K/AKT信号通路，发挥抑制烧伤休克血管内皮细胞凋亡的作用。因此，本项目拟分别过表达/沉默hMSC中的VEGF和miR-4793-3p，通过动物实验研究miR-4793-3p调控hMSC旁分泌VEGF，发挥抑制血管内皮凋亡和治疗烧伤休克的作用；通过细胞实验深入探讨miR-4793-3p对VEGF及其下游PI3K/AKT信号通路的调控影响，从而阐明hMSC抑制烧伤休克血管内皮细胞凋亡的分子机制。丰富hMSC的再生修复机制，为其的临床应用奠定理论基础。

The collapse of the effctive circulating blood volume caused by apoptosis of vascular endothelial cells is a pathophysiological basis of burn shock. However, there is currently no effective method about protective method of injured vascular endothelial cells. Shock is still the focus of burn treatment. Previous studies have shown that miR-4793-3p in hMSC could be down-regulated by burn shock serum. The miR-4793-3p has been proved to have a target-regulating effect on VEGF mRNA and an inhibiting effect on endothelial cells apoptosis induced by burn shock serum. But the mocular mechanisms of these effects are still unclear. Therefore, our team has hypothesized that miR-4793-3p could regulate hMSC to produce and paracrine VEGF, which could inhibit apoptosis of vascular endothelial cells induced by burn shock via activating PI3K/AKT signaling pathway. This project is designed to reveal the mechanisms of miR-4793-3p regulating hMSC to produce and paracrine VEGF, which inhibits apoptosis of vascular endothelial cells in animal and cell models of burn shock through overexpressing and silencing miR-4793-3p orVEGF. This study might provide a theoretical basis of the clinical application of hMSC.