We investigate the protective effect of ginsenoside Rb3 on skin flap microvasculature following ischemia-reperfusion (I/R) injury and its regulatory mechanism. We used a rat model of I/R injury with the right iliolumbar artery and oxidative stress model of human dermal microvascular endothelial cells. The effects of Rb3 on skin flap tissue and endothelial cell survival, STING-IRF3 pathway activation, and endothelial cell adhesion were measured. Following reperfusion, the survival rate of rat perforator flaps in the Rb3-treated group gradually increased with increasing Rb3 concentration. The treatment also reduced the amount of STING protein, phosphorylated IRF3, and P-selectin in skin flap tissue, with this change being most obvious in microvascular endothelial cells. In vitro, activated IRF3 binds to the P-selectin promoter and induces P-selectin expression. Our results suggest that Rb3 plays a role in reducing I/R flap damage through negatively regulating STING-IRF3 activation to limit leukocyte-endothelial cell adhesion.

我们研究了人参皂甙 Rb3 对缺血再灌注 (I/R) 损伤后皮瓣微血管的保护作用及其调节机制。我们使用右髂腰动脉的大鼠 I/R 损伤模型和人真皮微血管内皮细胞的氧化应激模型。测量了 Rb3 对皮瓣组织和内皮细胞存活、STING-IRF3 通路激活和内皮细胞粘附的影响。再灌注后，Rb3处理组大鼠穿支皮瓣的存活率随着Rb3浓度的增加而逐渐增加。该治疗还减少了皮瓣组织中 STING 蛋白、磷酸化 IRF3 和 P-选择素的数量，这种变化在微血管内皮细胞中最为明显。体外，激活的 IRF3 与 P-选择素启动子结合并诱导 P-选择素表达。我们的研究结果表明，Rb3 通过负调节 STING-IRF3 激活来限制白细胞-内皮细胞粘附，从而在减少 I/R 皮瓣损伤方面发挥作用。