【摘要】：目的:觀察5-羥色胺轉(zhuǎn)運(yùn)體(serotonin transporter,5-HTT)在慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)誘導(dǎo)的肺動(dòng)脈高壓(pulmonary hypertension,PH)大鼠肺組織中的表達(dá),探討5-HTT在PH發(fā)病中的作用及辛伐他汀對(duì)其的影響。方法:采用煙熏法建立PH動(dòng)物模型。將30只SD大鼠隨機(jī)分為三個(gè)組:對(duì)照組(control group)、煙霧暴露組(smoke exposure group)及辛伐他汀組(simvastatin group)。除control group外,另外兩組大鼠每一天在煙箱內(nèi)煙霧暴露2次,每次吸20支香煙,每次吸煙1h,共16周,自煙霧暴露之日起simvastatin group給予辛伐他汀(5mg/kg)灌胃治療,每日一次。16周后,測(cè)量大鼠的體重及肺動(dòng)脈壓(pulmonary artery pressure,PAP),并進(jìn)行肺組織病理形態(tài)學(xué)觀察;采用免疫組化方法對(duì)大鼠肺組織5-HTT蛋白進(jìn)行檢測(cè);應(yīng)用Real-Time PCR方法對(duì)肺組織中5-HTT的表達(dá)進(jìn)行測(cè)定;應(yīng)用western blot方法對(duì)大鼠肺組織5-HTT蛋白進(jìn)行檢測(cè),并觀察辛伐他汀對(duì)其表達(dá)的影響。結(jié)果:實(shí)驗(yàn)前,三組大鼠的體重?zé)o明顯差異(P0.05)。實(shí)驗(yàn)結(jié)束時(shí),smoke exposure group大鼠體重較control group明顯下降(P0.01);simvastatin group大鼠體重較control group明顯下降(P0.01),較smoke exposure group體重增加,兩者有統(tǒng)計(jì)學(xué)意義(P0.01);smoke exposure group m PAP相對(duì)于control group,顯著增高(P0.01)。simvastatin group m PAP較control group大鼠顯著增高(P0.01),較smoke exposure groupm PAP降低(P0.01);應(yīng)用免疫組化方法觀察5-HTT在肺組織中的表達(dá)。與control group比較,smoke exposure group中5-HTT蛋白表達(dá)升高,與smoke exposure group比較,辛伐他汀治療后5-HTT蛋白表達(dá)降低;應(yīng)用RT-PCR檢測(cè)大鼠肺組織中5-HTT m RNA的表達(dá)。smoke exposure group 5-HTT m RNA的表達(dá)較control group升高(P0.01),是control group的 (7.43±3.54)倍。simvastatin group 5-HTT m RNA的表達(dá)較control group升高(P0.01),是control group的(2.81±0.82)倍;應(yīng)用Western blot方法檢測(cè)大鼠肺組織中5-HTT蛋白的表達(dá)情況。smoke exposure group5-HTT蛋白的表達(dá)較control group升高,simvastatin group較control group升高較smoke exposure group降低。結(jié)論:1大鼠香煙煙霧暴露16周建立PH動(dòng)物模型成功。2 5-HTT在PH發(fā)生、發(fā)展過(guò)程中有明顯的變化及聯(lián)系,在PH發(fā)生發(fā)展中起重要作用。辛伐他汀可能是治療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 鹵3.54) times higher than that in control group (P0.01) and (2.81 鹵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.
【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類號(hào)】：R544.1

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