当归补血微囊促血管新生中JAK2/STAT3通路的作用研究

目的 探讨JAK2/STAT3信号传导通路在当归补血微囊促血管新生中的作用。方法 建立人脐静脉血管内皮细胞（HUVEC）模型，分别采用CCK-8和流式细胞术检测HUVEC细胞活力和细胞凋亡情况；采用Western blot检测各组中p-STAT3、VEGF的表达情况；采用荧光定量PCR，检测各组中VEGF基因和miRNA-21的表达情况。结果 20μg/mL当归补血微囊作用于HUVEC 24h，可有效促进HUVEC的增殖，并上调p-STAT3、VEGF及miRNA-21的表达；AG490能有效抑制当归补血微囊对HUVEC的促增殖作用，并减少p-STAT3、VEGF及miRNA-21的表达。结论 当归补血微囊促进血管生成的作用确实与JAK2/STAT3信号途径有关。 

Study on Function of JAK2/STAT3 Pathway in Promoting Angiogenesis with Angelica Microcapsules for Replenishing Blood

OBJECTIVE To investigate the function of JAK2/STAT3 pathway in promoting angiogenesis with Angelica microcapsules for replenishing blood (Ang-Mc). METHODS Establish the human umbilical vein endothelial cell (HUVEC) model， and then cell counting kit (CCK-8) and flow cytometry were used to test cell viability and cell apoptosis. Western blot was used to detect expression of p-STAT3 and VEGF. RT-PCR was used to detect expression of vascular endothelial growth factor (VEGF) and miRNA-21. RESULTS When Ang-Mc with a concentration of 20μg/mL acted on HUVEC for 24h， it could effectively promote the HUVEC proliferation by up-regulating the expression of p-STAT3， VEGF and miRNA-21. AG490 can effectively inhibit Ang-Mc promoting HUVEC proliferation effect and reduce the expression of p-STAT3， VEGF and miRNA-21. CONCLUSION The effect of Ang-Mc in promoting angiogenesis is related to JAK2/STAT3 signaling pathways.