丹酚酸B通过激活TFE3介导的自噬发挥对随机皮瓣的保护作用

Alvianolic acid B exerts a protective effect on random skin flaps through autophagy mediated by activation of TFE3

目的观察丹酚酸B(salvianolic acid B,Sal B)促进随机皮瓣存活的作用并初步探讨其可能的机制。方法采用外科手术构建随机皮瓣模型,术后7 d评估皮瓣的外观、水肿程度、颜色和毛发状况。激光多普勒血流测量技术检测随机皮瓣血管网络和血流量;HE染色检测随机皮瓣微血管生长情况;免疫组化检测促血管生成因子VEGF、CD34的表达,免疫荧光检测RIPK1、2和LC3Ⅱ的表达,Western blot检测自噬相关蛋白以及信号通路的影响。结果Sal B诱导了随机皮瓣的自噬,促进了血管生成,并减少了坏死性凋亡的发生,显著增加了随机皮瓣的存活率。免疫组化、免疫荧光染色和Western blot检测等实验证实,Sal B通过激活TFE3蛋白诱导了随机皮瓣发生自噬。结论Sal B可通过激活TFE3蛋白促进随机皮瓣细胞发生自噬并降低其坏死凋亡。

Aim To observe the role of salvianolic acid B(Sal B)in enhancing the survival of random skin flaps and to preliminarily explore its potential mechanisms.Methods The appearance,degree of edema,color and hair condition of the skin flap were evaluated seven days after operation.The vascular network and blood flow of random flaps were measured by laser Doppler flow measurement.HE staining was used to detect the growth of microvessels in random flaps.The expressions of VEGF and CD34 were detected by immunohistochemistry,the expressions of RIPK1,2 and LC3Ⅱwere detected by immunofluorescence,and the effects of autophagy related proteins and signaling pathways were detected by Western blot.Results The experimental results showed that Sal B induced autophagy in the random skin flaps,promoted angiogenesis,and reduced oxidative stress and necrotic apoptosis,significantly increasing the survival rate of the flaps.Immunohistochemistry,immunofluorescence staining,and Western blot confirmed that Sal B induced autophagy in the random skin flaps by activating TFE3 protein.Conclusion Sal B can promote autophagy in cells of random skin flaps and reduce their necrotic apoptosis by activating TFE3 protein.