HIF-1-VEGF通路在SMVT大鼠肠道组织中的表达及意义

发布时间：2018-05-27 13:10

本文选题：肠系膜上静脉血栓形成 + 低氧诱导因子-1α　；参考：《华北理工大学》2017年硕士论文

【摘要】：目的观察HIF-1-VEGF通路信号分子在大鼠肠系膜上静脉血栓形成(Superior mesenteric venous thrombosis,SMVT)肠道组织中的表达,探讨该通路在SMVT中的作用。方法1 64只雄性SD大鼠,随机分为两组,假手术组(Sham组)和实验组(SMVT组),每组大鼠32只。2 Sham组:仅打开腹腔,不阻断血运,术后8h、24h、48h、72h分批处死大鼠;SMVT组:结扎法建立单纯性周围型SMVT模型,建模后8h、24h、48h、72h分批处死大鼠。3观察腹腔及肠道大体变化;HE染色观察大鼠肠道组织病理学变化;Real-time q PCR检测大鼠肠道组织HIF-1α及VEGF m RNA的表达;免疫组织化学染色及Western blot检测大鼠肠道组织HIF-1α及VEGF蛋白的表达。结果1大体观察结果显示:Sham组腹腔及肠道未见明显变化;SMVT组大鼠腹腔出现不同程度及不同性状积液,静脉呈不同程度的怒张状态,肠道呈不同程度的肿胀及血液瘀滞状态,且均随时间延长而逐渐减轻。2 HE染色结果显示:Sham组大鼠肠道组织均无明显病理变化;SMVT组大鼠肠道组织均出现不同程度红细胞瘀滞,且随时间延长瘀滞程度逐渐减轻。3 Real-time q PCR结果显示:SMVT组较Sham组对应各时间点HIF-1α及VEGF m RNA表达明显升高(P0.05),且均呈递减趋势。4免疫组织化学染色及Western blot结果显示:SMVT组较Sham组对应各时间点HIF-1α及VEGF蛋白表达明显升高(P0.05),且均呈先升后降趋势。结论1 SMVT发病后,HIF-1α表达增加,并通过对其下游靶基因VEGF进行调控,启动血管新生和生长过程,对缺血肠道组织侧枝循环的建立具有重要意义。2SMVT发病后,VEGF在HIF-1α的调控下表达增加,促进血管的新生和生长,对缺血肠道组织侧枝循环的建立具有促进作用。3 SMVT发病后,肠道组织缺血缺氧激活HIF-1-VEGF通路,信号分子HIF-1α及VEGF表达同步增加,促进血管新生和生长,加速侧枝循环的建立,减轻血液瘀滞及微循环障碍,减少透壁性肠梗死的发生。
[Abstract]:Objective to investigate the expression of HIF-1-VEGF signaling molecule in the intestinal tissues of superior mesenteric venous thrombosis (SMBT) in rats, and to explore the role of this pathway in SMVT. Methods Sixty-four male Sprague-Dawley rats were randomly divided into two groups: sham-operated group (Sham group) and experimental group (32 rats in Sham group). The rats were killed in batches at 8 h, 24 h, 48 h and 72 h after operation. The simple peripheral SMVT model was established by ligation. Rats were sacrificed in batches at 8 h, 24 h, 48 h and 72 h to observe the gross changes of abdominal cavity and intestine. The histopathological changes of intestinal tissue were observed by HE staining. Real-time Q PCR was used to detect the expression of HIF-1 伪 and VEGF m RNA in rat intestinal tissue. Immunohistochemical staining and Western blot were used to detect the expression of HIF-1 伪 and VEGF protein in rat intestinal tissue. Results 1 the results of gross observation showed that there were no obvious changes in abdominal cavity and intestine of rats in the control group. In SMVT group, there were different degrees of effusion in abdominal cavity, different degree of irritation in vein, and different degree of swelling and blood stasis in intestinal tract of SMVT group. The results of HE staining showed that there were no obvious pathological changes in intestinal tissue of rats in the control group. All the intestinal tissues of SMVT group had different degrees of erythrocyte stasis. The results showed that the expression of HIF-1 伪 and VEGF m RNA in the Sham group was significantly higher than that in the Sham group, and the expression of HIF-1 伪 and VEGF m RNA in the Sham group was significantly higher than that in the Sham group. The expression of HIF-1 伪 and VEGF m RNA in the Sham group was significantly higher than that in the control group. 4. 4 immunohistochemical staining and Western blot showed that the HIF-1 伪 and VEGF m RNA expression in the Sham group were significantly higher than those in the control group. Compared with Sham group, the expression of HIF-1 伪 and VEGF protein increased significantly at each time point, and the expression of HIF-1 伪 and VEGF protein increased first and then decreased. Conclusion (1) the expression of HIF-1 伪 is increased after the onset of SMVT. By regulating the downstream target gene VEGF and initiating the process of angiogenesis and growth, it is important for the establishment of collateral circulation in ischemic intestinal tissue to increase the expression of SMVT under the control of HIF-1 伪. Promoting angiogenesis and growth, promoting the establishment of collateral circulation of intestinal tissue after 3. 3 SMVT, intestinal ischemia and hypoxia activated HIF-1-VEGF pathway, the expression of signal molecules HIF-1 伪 and VEGF increased synchronously, and promoted angiogenesis and growth. Accelerate the establishment of collateral circulation, reduce blood stasis and microcirculation, reduce the incidence of transmural intestinal infarction.
【学位授予单位】：华北理工大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R572.3

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