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目的:探讨P311对人微血管内皮细胞1（HMEC-1）血管形成能力的影响及其可能的分子机制。方法:采用实验研究方法。取HMEC-1，按随机数字表法（分组方法下同）分为P311腺病毒组和空载腺病毒组，分别进行48 h相应转染后，采用细胞计数试剂盒8法检测培养1、3、5 d细胞增殖活性；划痕试验检测细胞划痕后6、11 h剩余划痕面积，并计算剩余划痕面积百分比；体外血管形成实验观察细胞培养8 h血管形成情况，并测量管状结构节点数和总长度；蛋白质印迹法检测细胞中血管内皮生长因子受体2（VEGFR2）、磷酸化VEGFR2、胞外信号调节激酶1/2（ERK1/2）及磷酸化ERK1/2蛋白表达量。取HMEC-1，分为P311腺病毒+阴性对照小干扰RNA（siRNA）组、空载腺病毒+阴性对照siRNA组、P311腺病毒+siRNA-VEGFR2组和空载腺病毒+siRNA-VEGFR2组，分别进行相应的处理，蛋白质印迹法检测转染24 h细胞中VEGFR2、磷酸化VEGFR2、ERK1/2、磷酸化ERK1/2蛋白表达量；体外血管形成实验观察转染24 h细胞血管形成情况，并测量管状结构节点数和总长度。取HMEC-1，分为P311腺病毒+二甲基亚砜（DMSO）组、空载腺病毒+DMSO组、P311腺病毒+ERK1/2抑制剂组和空载腺病毒+ERK1/2抑制剂组，分别进行相应的处理。蛋白质印迹法检测处理2 h细胞中ERK1/2及磷酸化ERK1/2蛋白表达量；体外血管形成实验观察处理2 h细胞血管形成情况，并测量管状结构节点数和总长度。各组各时间点样本数均为6。对数据行独立样本n t检验、重复测量方差分析、单因素方差分析、LSD检验。n 结果:与空载腺病毒组比较，P311腺病毒组细胞培养1、3、5 d增殖活性均没有明显改变（n t值分别为-0.23、-1.30、-1.52，n P>0.05）。P311腺病毒组细胞划痕后6、11 h剩余划痕面积百分比均较空载腺病毒组明显降低（n t值分别为-2.47、-2.62，n P<0.05）。培养8 h，与空载腺病毒组比较，P311腺病毒组细胞管状结构节点数和总长度均明显增加（n t值分别为4.49、4.78，n P0.05），磷酸化VEGFR2、磷酸化ERK1/2蛋白表达量均明显升高（n t值分别为17.27、16.08，n P<0.01）。转染24 h，P311腺病毒+阴性对照siRNA组细胞磷酸化VEGFR2和磷酸化ERK1/2蛋白表达量均明显高于空载腺病毒+阴性对照siRNA组（n P<0.01），P311腺病毒+阴性对照siRNA组细胞VEGFR2、磷酸化VEGFR2、磷酸化ERK1/2蛋白表达量均明显高于P311腺病毒+siRNA-VEGFR2组（n P<0.01），空载腺病毒+阴性对照siRNA组细胞VEGFR2、磷酸化ERK1/2蛋白表达量均明显高于空载腺病毒+siRNA-VEGFR2组（n P<0.05或n P<0.01）。转染24 h，P311腺病毒+阴性对照siRNA组细胞管状结构节点数为（720±62）个，明显多于空载腺病毒+阴性对照siRNA组的（428±38）个、P311腺病毒+siRNA-VEGFR2组的（364±57）个（n P值均<0.01）；P311腺病毒+阴性对照siRNA组细胞管状结构总长度为（21 241±1 139）μm，明显长于空载腺病毒+阴性对照siRNA组的（17 005±1 156）μm、P311腺病毒+siRNA-VEGFR2组的（13 494±2 465）μm（n P值均<0.01）。空载腺病毒+阴性对照siRNA组细胞管状结构节点数明显多于空载腺病毒+siRNA-VEGFR2组的（310±75）个（n P<0.01），管状结构总长度明显长于空载腺病毒+siRNA-VEGFR2组的（11 600±2 776）μm（n P<0.01）。处理2 h，P311腺病毒+DMSO组细胞磷酸化ERK1/2蛋白表达量明显高于空载腺病毒+DMSO组、P311腺病毒+ERK1/2抑制剂组（n P值均<0.01），空载腺病毒+DMSO组细胞磷酸化ERK1/2蛋白表达量明显高于空载腺病毒+ERK1/2抑制剂组（n P<0.05）。处理2 h，P311腺病毒+DMSO组细胞管状结构节点数为（726±72）个，明显多于空载腺病毒+DMSO组的（421±39）个、P311腺病毒+ERK1/2抑制剂组的（365±41）个（n P值均<0.01）；P311腺病毒+DMSO组细胞管状结构总长度为（20 318±1 433）μm，明显长于空载腺病毒+DMSO组的（16 846±1 464）μm、P311腺病毒+ERK1/2抑制剂组的（15 114±1 950）μm（n P值均<0.01）。空载腺病毒+DMSO组管状结构节点数明显多于空载腺病毒+ERK1/2抑制剂组的（317±67）个（n P<0.01），管状结构总长度明显长于空载腺病毒+ERK1/2抑制剂组的（13 188±2 306）μm（n P0.05). The residual scratch area percentages of cells in P311 adenovirus group were significantly reduced at post scratch hour 6 and 11 compared with those of empty adenovirus group (withn t values of -2.47 and -2.62, respectively, n P<0.05). At 8 h of culture, compared with those of empty adenovirus group, the number of nodes and total length of the tubular structure of cells in P311 adenovirus group were significantly increased (withn t values of 4.49 and 4.78, respectively, n P0.05), and the protein expressions of p-VEGFR2 and p-ERK1/2 of cells in P311 adenovirus group were significantly increased (withn t values of 17.27 and 16.08, n P<0.01). At 24 h of transfection, the protein expressions of p-VEGFR2 and p-ERK1/2 of cells in P311 adenovirus+siRNA negative control group were significantly higher than those in empty adenovirus+siRNA negative control group (n P<0.01). The protein expressions of VEGFR2, p-VEGFR2, and p-ERK1/2 of cells in P311 adenovirus+siRNA negative control group were significantly higher than those in P311 adenovirus+siRNA-VEGFR2 group (n P<0.01). The protein expressions of VEGFR2 and p-ERK1/2 of cells in empty adenovirus+siRNA negative control group were significantly higher than those in empty adenovirus+siRNA-VEGFR2 group (n P<0.05 orn P<0.01). At 24 h of transfection, the number of nodes of the tubular structure in cells of P311 adenovirus+siRNA negative control group was 720±62, which was significantly more than 428±38 in empty adenovirus+siRNA negative control group and 364±57 in P311 adenovirus+siRNA-VEGFR2 group (withn P values both <0.01). The total length of the tubular structure of cells in P311 adenovirus+siRNA negative control group was (21 241±1 139) μm, which was significantly longer than (17 005±1 156) μm in empty adenovirus+siRNA negative control group and (13 494±2 465) μm in P311 adenovirus+siRNA-VEGFR2 group (with n P values both <0.01). The number of nodes of the tubular structure in cells of empty adenovirus+siRNA negative control group was significantly more than 310±75 in empty adenovirus+siRNA-VEGFR2 group ( n P<0.01), and the total length of the tubular structure of cells in empty adenovirus+siRNA negative control group was significantly longer than (11 600±2 776) μm in empty adenovirus+siRNA-VEGFR2 group (n P<0.01). At 2 h of treatment, the protein expression of p-ERK1/2 of cells in P311 adenovirus+DMSO group was significantly higher than that in empty adenovirus+DMSO group and P311 adenovirus+ERK1/2 inhibitor group (withn P values both <0.01), and the protein expression of p-ERK1/2 of cells in empty adenovirus+DMSO group was significantly higher than that in empty adenovirus+ERK1/2 inhibitor group ( n P<0.05). At 2 h of treatment, the number of nodes of the tubular structure in cells of P311 adenovirus+DMSO group was 726±72, which was significantly more than 421±39 in empty adenovirus+DMSO group and 365±41 in P311 adenovirus+ERK1/2 inhibitor group (withn P values both <0.01). The total length of the tubular structure of cells in P311 adenovirus+DMSO group was (20 318±1 433) μm, which was significantly longer than (16 846±1 464) μm in empty adenovirus+DMSO group and (15 114±1 950) μm in P311 adenovirus+ERK1/2 inhibitor group (with n P values both <0.01). The number of nodes of the tubular structure in cells of empty adenovirus+DMSO group was significantly more than 317±67 in empty adenovirus+ERK1/2 inhibitor group ( n P<0.01), and the total length of the tubular structure of cells in empty adenovirus+DMSO group was significantly longer than (13 188±2 306) μm in empty adenovirus+ERK1/2 inhibitor group (n P<0.01).n Conclusions:P311 can enhance the angiogenesis ability of HMEC-1 by activating the VEGFR2/ERK1/2 signaling pathway.