当归补血微囊促血管新生中JAK2/STAT3通路的作用研究

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

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pSTAT3、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 20μg/mL当归补血微囊作用于HUVEC 24h,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。

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 20μg/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.