目的:探讨不同剂量紫草素对雌激素加孕激素负荷法建立的子宫肌瘤大鼠的子宫组织ER、PR和p-ERK的蛋白表达影响.方法:选择清洁级SD雌性大鼠60只,将其分为模型组、空白对照组、阳性对照组(雌二醇组)、低剂量紫草素组、中剂量紫草素组、高剂量紫草素组,每组10只大鼠.空白对照组、模型组大鼠给大鼠灌胃10 mL/kg·d生理盐水,阳性对照组给予戊酸雌二醇雌片灌胃,剂量为50 μg/kg·d,低剂量组灌胃给予5 mg/kg紫草素,中剂量组灌胃给予10 mg/kg紫草素,高剂量组灌胃给予20 mg/kg紫草素.记录大鼠的造模结果,观察大鼠的子宫形态、子宫病理组织学情况,对比各组大鼠的子宫重量、子宫系数、宫体最大直径、宫颈最大直径及平滑肌层厚度,检测每组大鼠的血清P、E2水平及各组大鼠子宫组织ER、PR、p-ERK蛋白含量.结果:六组大鼠的子宫重量、子宫系数、宫体最大直径、宫颈最大直径及平滑肌层厚度指标两两比较,差异有统计学意义(P＜0.05);六组大鼠的炎性细胞浸润评分及子宫壁平滑肌厚度评分两两比较,差异有统计学意义(P＜0.05);六组大鼠的血清P、E2水平两两比较,差异有统计学意义(P＜0.05);六组大鼠的子宫组织ER、PR、p-ERK蛋白水平两两比较,差异有统计学意义(P＜0.05).结论:紫草素具有抗子宫肌瘤活性的作用,随着紫草素剂量的增加,抗子宫肌瘤活性明显增加,可能与其可降低子宫组织ER、PR和p-ERK活性及血清P、E2水平有关.

目的:探究人羊膜上皮干细胞(hAECs)联合富血小板血浆(PRP)对宫腔粘连大鼠的治疗效果,为临床中优化宫腔粘连治疗方法理论基础.方法:选用SPF级雌性SD大鼠共40只,依照随机数字表法随机分为空白组(A组)、假手术组(B组)、hAECs组(C组)、PRP组(D组)、hAECs+PRP组(E组),每组各8只.A组不做任何处理,B组仅做麻醉、开关腹腔处理,C组、D组、E组使用搔刮法制备宫腔粘连模型.随后C组进行hAECs治疗,D组注射等量生理盐水.D组进行PRP治疗,C组注射等量生理盐水.E组进行hAECs联合PRP治疗.观察比较两组大鼠子宫内膜组织基质金属蛋白酶-9(MMP-9)、盘状结构域受体2(DDR2)蛋白表达水平、PI3K/Akt/mTOR通路相关mRNA表达量、血清白细胞介素-6(IL-6)、白细胞介素-8(IL-8)水平以及各组大鼠妊娠孕囊数量比较.结果:与A组相比,B组的子宫内膜组织MMP-9、DDR2蛋白表达水平、p-mTORmRNA、p-AktmRNA水平以及血清IL-6、IL-8水平比较无差异(P＞0.05);C组、D组、E组大鼠的子宫内膜组织MMP-9、DDR2蛋白表达水平明显下降,IL-6、IL-8水平、p-mTORmRNA、p-AktmRNA表达升高(P＜0.05).其中,E组大鼠MMP-9、DDR2蛋白表达水平明显高于C组、D组,IL-6、IL-8水平及p-mTORmRNA、p-AktmRNA表达低于C组、D组(P＜0.05).C组、D组大鼠MMP-9、DDR2蛋白表达水平、血清IL-6、IL-8水平及p-mTOR mRNA、p-Akt mRNA表达比较(P＞0.05).妊娠孕囊数量方面,与A组比较,B组大鼠妊娠孕囊数量.结论:hAECs联合PRP治疗可能通过上调宫腔粘连大鼠子宫内膜组织MMP-9、DDR2蛋白表达水平并下调p-mTORmRNA、p-Akt mRNA表达,同时降低炎性因子IL-6、IL-8水平,进而提高妊娠孕囊数量,起到治疗作用.

Objective To investigate the mechanism of miR-451 regulating the resistance of gastric cancer to 5-Fu by down-regulating the expression of MRP. Methods Real-time quantitative PCR was used to detect the relative expression of miR-451 in 20 pairs of human gastric cancer tissues and adjacent tissues and gastric cancer cell lines. The expression of miR-451 in the resistance group and non-resistant group were detected. We constructed gastric cancer cell line with stable plent-miR-451 overexpression, and the overexpression efficiency of miR-451 in gastric cancer cell line was detected by real-time quantitative PCR. The proliferation activity of the cells was detected by CCK8. The miR-451 target gene was analyzed by bioinformatics method and verified by luciferase assay. The effect of miR-451 on the mRNA and protein of targeted gene MRP were detected by real-time quantitative PCR and Western blot. Results The expression of miR-451 in normal tissues was higher than that in cancer tissues, and miR-451 expression in the non-resistant gastric cancer tissues was higher than that in the drug-resistant gastric cancer tissues. The overexpression of miR-451 reduced the resistance of gastric cancer cells to 5-Fu treatment (P=0.0006). Bioinformatics analysis showed that MRP was the target gene of miR-451. Luciferase assay also confirmed that MRP was a potential target gene of miR-451. miR-451 overexpression decreased the mRNA and protein of the drug resistance gene MRP (P=0.00069). Conclusion Overexpression of miR451 could down-regulate MRP expression, which reduces the resistance of tumor cells to 5-Fu.

目的:探讨多分子靶向药物索拉菲尼对体外培养人子宫内膜癌细胞(HEC-1B)增殖、凋亡的影响.方法:MTT检测细胞活力/增殖情况,免疫印迹检测细胞内caspase3蛋白水平;流式细胞仪检测细胞凋亡;对比阴性对照组(正常培养的细胞),分析索拉菲尼对子宫内膜癌细胞增殖/凋亡的影响.结果:索拉菲尼对子宫内膜癌细胞增殖有抑制作用,且随着药物浓度增加作用也增强(P＜0.05);与对照组相比,索拉菲尼处理组细胞caspase3蛋白表达及凋亡率均明显增加(P＜0.05).结论:索拉菲尼对体外培养的人子宫内膜癌细胞有明显的抑制作用.

目的:研究雌激素及其拮抗剂对人胃腺癌SGC-7901细胞系血管内皮细胞生长因子(VEGF)表达的影响.方法:用雌二醇及其拮抗剂三苯氧胺(tamoxifen)处理体外培养的胃癌细胞系SGC-7901,在相差显微镜下观察细胞形态的变化;用四甲基偶氮唑蓝(MTT)比色法测定细胞增殖;用双抗体夹心酶联免疫吸附试验(ELISA)和免疫细胞化学SABC法测定细胞培养上清液和细胞质中VEGF蛋白含量.结果:胃癌细胞经雌二醇处理,培养液中VEGF浓度明显高于对照组(P＜0.05);而雌二醇加三苯氧胺联合处理胃癌细胞,VEGF浓度有回降,比雌二醇处理组下降.结论:提示雌激素参与调节胃癌细胞VEGF的表达浓度,三苯氧胺有抑制VEGF表达的作用.