肺动脉高压大鼠5-HTT的表达及辛伐他汀对其的影响
发布时间：2019-01-06 06:36
【摘要】：目的:观察5-羟色胺转运体(serotonin transporter,5-HTT)在慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)诱导的肺动脉高压(pulmonary hypertension,PH)大鼠肺组织中的表达,探讨5-HTT在PH发病中的作用及辛伐他汀对其的影响。方法:采用烟熏法建立PH动物模型。将30只SD大鼠随机分为三个组:对照组(control group)、烟雾暴露组(smoke exposure group)及辛伐他汀组(simvastatin group)。除control group外,另外两组大鼠每一天在烟箱内烟雾暴露2次,每次吸20支香烟,每次吸烟1h,共16周,自烟雾暴露之日起simvastatin group给予辛伐他汀(5mg/kg)灌胃治疗,每日一次。16周后,测量大鼠的体重及肺动脉压(pulmonary artery pressure,PAP),并进行肺组织病理形态学观察;采用免疫组化方法对大鼠肺组织5-HTT蛋白进行检测;应用Real-Time PCR方法对肺组织中5-HTT的表达进行测定;应用western blot方法对大鼠肺组织5-HTT蛋白进行检测,并观察辛伐他汀对其表达的影响。结果:实验前,三组大鼠的体重无明显差异(P0.05)。实验结束时,smoke exposure group大鼠体重较control group明显下降(P0.01);simvastatin group大鼠体重较control group明显下降(P0.01),较smoke exposure group体重增加,两者有统计学意义(P0.01);smoke exposure group m PAP相对于control group,显著增高(P0.01)。simvastatin group m PAP较control group大鼠显著增高(P0.01),较smoke exposure groupm PAP降低(P0.01);应用免疫组化方法观察5-HTT在肺组织中的表达。与control group比较,smoke exposure group中5-HTT蛋白表达升高,与smoke exposure group比较,辛伐他汀治疗后5-HTT蛋白表达降低;应用RT-PCR检测大鼠肺组织中5-HTT m RNA的表达。smoke exposure group 5-HTT m RNA的表达较control group升高(P0.01),是control group的 (7.43±3.54)倍。simvastatin group 5-HTT m RNA的表达较control group升高(P0.01),是control group的(2.81±0.82)倍;应用Western blot方法检测大鼠肺组织中5-HTT蛋白的表达情况。smoke exposure group5-HTT蛋白的表达较control group升高,simvastatin group较control group升高较smoke exposure group降低。结论:1大鼠香烟烟雾暴露16周建立PH动物模型成功。2 5-HTT在PH发生、发展过程中有明显的变化及联系,在PH发生发展中起重要作用。辛伐他汀可能是治疗PH有效的方法之一。
[Abstract]:Aim: to investigate the expression of serotonin transporter (serotonin transporter,5-HTT) in pulmonary artery hypertension (pulmonary hypertension,PH) induced by chronic obstructive pulmonary disease (chronic obstructive pulmonary disease,COPD) in rats. To investigate the role of 5-HTT in the pathogenesis of PH and the effect of simvastatin on it. Methods: PH animal model was established by smoking. Thirty SD rats were randomly divided into three groups: control group, (control group), smoke exposure group, (smoke exposure group) group, and simvastatin group, (simvastatin group). Group. In addition to control group, the other two groups of rats were exposed to smoke in the cigarette box twice a day, smoking 20 cigarettes for 1 hour each time for 16 weeks. Since the day of smoke exposure, simvastatin group was given intragastric administration of Simvastatin (5mg/kg). Body weight and pulmonary artery pressure (pulmonary artery pressure,PAP) were measured once a day for 16 weeks, and lung histopathology was observed. Immunohistochemical method was used to detect 5-HTT protein in rat lung tissue, and Real-Time PCR method was used to detect the expression of 5-HTT in lung tissue. Western blot method was used to detect the expression of 5-HTT protein in rat lung and to observe the effect of simvastatin on its expression. Results: before the experiment, there was no significant difference in body weight among the three groups (P 0.05). At the end of the experiment, the weight of, smoke exposure group rats was significantly lower than that of control group (P0.01); simvastatin group rats were significantly lower than that of control group (P0.01), and the weight of smoke exposure group was higher than that of smoke exposure group (P0.01). Compared with control group, smoke exposure group m PAP increased significantly (P0.01). Simvastatin group m PAP was significantly higher than that of control group rats (P0.01), lower than that of smoke exposure groupm PAP (P0.01), and the expression of 5-HTT in lung tissue was observed by immunohistochemical method. Compared with control group, the expression of 5-HTT protein in, smoke exposure group was higher than that in smoke exposure group. Compared with smoke exposure group, the expression of 5-HTT protein decreased after simvastatin treatment. The expression of 5-HTT m RNA in rat lung tissue was detected by RT-PCR. The expression of. Smoke exposure group 5-HTT m RNA was higher than that of control group (P0.01). The expression of. Simvastatin group 5-HTT m RNA in control group was (7.43 卤3.54) times higher than that in control group (P0.01) and (2.81 卤0.82) times in control group. The expression of 5-HTT protein in rat lung tissue was detected by Western blot method. The expression of. Smoke exposure group5-HTT protein was higher than that of control group. The expression of, simvastatin group was higher than that of control group and the expression of. Smoke exposure group5-HTT was lower than that of smoke exposure group. Conclusion: 1 the animal model of rat cigarette smoke exposure to 16 Zhou Jianli PH was successful. 2 5-HTT had obvious changes and connections during the development of PH, and played an important role in the occurrence and development of PH. Simvastatin may be one of the effective treatments for PH.
【学位授予单位】：河北医科大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R544.1
[Abstract]:Aim: to investigate the expression of serotonin transporter (serotonin transporter,5-HTT) in pulmonary artery hypertension (pulmonary hypertension,PH) induced by chronic obstructive pulmonary disease (chronic obstructive pulmonary disease,COPD) in rats. To investigate the role of 5-HTT in the pathogenesis of PH and the effect of simvastatin on it. Methods: PH animal model was established by smoking. Thirty SD rats were randomly divided into three groups: control group, (control group), smoke exposure group, (smoke exposure group) group, and simvastatin group, (simvastatin group). Group. In addition to control group, the other two groups of rats were exposed to smoke in the cigarette box twice a day, smoking 20 cigarettes for 1 hour each time for 16 weeks. Since the day of smoke exposure, simvastatin group was given intragastric administration of Simvastatin (5mg/kg). Body weight and pulmonary artery pressure (pulmonary artery pressure,PAP) were measured once a day for 16 weeks, and lung histopathology was observed. Immunohistochemical method was used to detect 5-HTT protein in rat lung tissue, and Real-Time PCR method was used to detect the expression of 5-HTT in lung tissue. Western blot method was used to detect the expression of 5-HTT protein in rat lung and to observe the effect of simvastatin on its expression. Results: before the experiment, there was no significant difference in body weight among the three groups (P 0.05). At the end of the experiment, the weight of, smoke exposure group rats was significantly lower than that of control group (P0.01); simvastatin group rats were significantly lower than that of control group (P0.01), and the weight of smoke exposure group was higher than that of smoke exposure group (P0.01). Compared with control group, smoke exposure group m PAP increased significantly (P0.01). Simvastatin group m PAP was significantly higher than that of control group rats (P0.01), lower than that of smoke exposure groupm PAP (P0.01), and the expression of 5-HTT in lung tissue was observed by immunohistochemical method. Compared with control group, the expression of 5-HTT protein in, smoke exposure group was higher than that in smoke exposure group. Compared with smoke exposure group, the expression of 5-HTT protein decreased after simvastatin treatment. The expression of 5-HTT m RNA in rat lung tissue was detected by RT-PCR. The expression of. Smoke exposure group 5-HTT m RNA was higher than that of control group (P0.01). The expression of. Simvastatin group 5-HTT m RNA in control group was (7.43 卤3.54) times higher than that in control group (P0.01) and (2.81 卤0.82) times in control group. The expression of 5-HTT protein in rat lung tissue was detected by Western blot method. The expression of. Smoke exposure group5-HTT protein was higher than that of control group. The expression of, simvastatin group was higher than that of control group and the expression of. Smoke exposure group5-HTT was lower than that of smoke exposure group. Conclusion: 1 the animal model of rat cigarette smoke exposure to 16 Zhou Jianli PH was successful. 2 5-HTT had obvious changes and connections during the development of PH, and played an important role in the occurrence and development of PH. Simvastatin may be one of the effective treatments for PH.
【学位授予单位】：河北医科大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R544.1
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