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

  • 摘要: 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。

     

    Abstract: 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.

     

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