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目的研究益气消癥法方含药血清对EA.hy926细胞丝裂原活化蛋白激酶(MAPK)信号通路上细胞外信号调节激酶1/2(ERK1/2)表达的影响,探索其抑制子宫肌瘤血管新生的作用机制。方法 SD大鼠随机分为:对照组,益气消癥法方高、中、低剂量(生药剂量24、12、6 g/kg)组,ig给药,每天给药1次,连续给药5 d,腹主动脉取血,分离血清,灭活、过滤除菌;体外培养EA.hy926细胞,随机分为6组:对照血清组、模型组及益气消癥法方高、中、低剂量血清组和氟维司群(ICI,阳性药)组,除对照血清组外,其余组别给予雌二醇(E2),诱导细胞增殖,制备子宫肌瘤血管模型;通过实时荧光定量PCR(q RT-PCR)及Western blotting法检测MEK2和ERK1/2基因与蛋白的表达。结果模型组MEK2和ERK1/2基因与蛋白的表达水平明显高于对照血清组(P<0.01);与模型组比较,ICI和益气消癥法方高剂量血清组MEK2和ERK1/2表达水平显著降低(P<0.01)。结论益气消癥法方含药血清通过降调ERK1/2表达,阻断MAPK/ERK1/2信号转导,抑制雌激素诱导的血管内皮细胞增殖,减少子宫肌瘤血液供应。
Objective To investigate the effect of Yiqi Xiaoyan Prescription-containing serum on the expression of extracellular signal-regulated kinase 1/2 (ERK1 / 2) on mitogen-activated protein kinase (MAPK) signaling pathway in EA.hy926 cells and explore its inhibitory effect on uterine muscle The mechanism of tumor angiogenesis. Methods SD rats were randomly divided into control group, Yiqi Xiaozheng Fang high, medium and low doses (raw drug dose 24,12,6 g / kg) group, ig administration, once daily administration, continuous administration 5 d, blood was collected from the abdominal aorta, serum was isolated, inactivated, filtered and sterilized; EA.hy926 cells cultured in vitro were randomly divided into 6 groups: control serum group, Dose serum and fulvestrant (ICI, positive drug) group, in addition to the control serum group, the other groups were given estradiol (E2), induced cell proliferation, preparation of uterine fibrovascular model; by real-time quantitative PCR q RT-PCR) and Western blotting were used to detect the expression of MEK2 and ERK1 / 2 genes and proteins. Results The expression of MEK2 and ERK1 / 2 gene and protein in the model group was significantly higher than that in the control serum group (P <0.01). Compared with the model group, the expression levels of MEK2 and ERK1 / 2 in ICI and Yiqi Xiezheng high-dose serum group Significantly lower (P <0.01). Conclusion Yiqi Xiaozheng Prescription-containing serum can inhibit the signal transduction of MAPK / ERK1 / 2, decrease the estrogen-induced proliferation of vascular endothelial cells and decrease the blood supply of uterine fibroids by decreasing ERK1 / 2 expression.