本文選題：煙霧暴露 + 高血壓��； 參考：《山西醫(yī)科大學(xué)》2013年碩士論文

【摘要】：目的：研究煙霧暴露對(duì)大鼠肺組織血小板衍生生長(zhǎng)因子-BB (Platelet derived growth factor-BB, PDGF-BB)和核因子-kB(nuclear factor-KB, NF-kB)p65表達(dá)的影響,探討煙霧暴露致大鼠肺動(dòng)脈高壓的發(fā)生機(jī)制。 方法：雄性Wistar大鼠32只,隨機(jī)分為對(duì)照組、煙霧暴露4、8、12周組,每組8只,制備煙霧暴露組肺動(dòng)脈高壓模型。將煙霧暴露組大鼠置于自制實(shí)驗(yàn)性大鼠被動(dòng)吸煙箱內(nèi)進(jìn)行被動(dòng)吸煙,分別煙霧暴露4、8、12周,對(duì)照組除無(wú)煙霧暴露外,其他條件完全相同。各組大鼠模型制備成功后,右心導(dǎo)管法測(cè)大鼠肺動(dòng)脈平均壓(mean pulmonary arterial pressure, mPAP),無(wú)菌條件下完整游離心、肺組織,計(jì)算大鼠右心肥厚指數(shù)(right ventricle hypertrophy index, RVHI),取左肺組織置于-80℃冰箱凍存,用RT-PCR測(cè)各組大鼠肺組織mRNA的相對(duì)表達(dá)量,取右肺組織常規(guī)石蠟包埋、切片,用于HE染色,免疫組織化學(xué)染色法測(cè)各組大鼠肺組織中PDGF-BB及NF-KBp65蛋白的表達(dá),分析各指標(biāo)的相關(guān)性。 結(jié)果：①大鼠肺組織中PDGF-BB mRNA相對(duì)表達(dá)量在煙霧暴露12周組(6.098±0.439)及8周組(4.015±0.052)高于4周組(2.823±0.453)及對(duì)照組(1.024±0.231),差異有統(tǒng)計(jì)學(xué)意義(P均0.05)；煙霧暴露12周組(6.098±0.439)高于8周組(4.015±0.052),差異有統(tǒng)計(jì)學(xué)意義(P0.05)；煙霧暴露4周組與對(duì)照組組間差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)；②大鼠肺組織中PDGF-BB蛋白相對(duì)表達(dá)量在煙霧暴露4周組(0.220±0.005)、8周組(0.367±0.004)、12周組(0.492±0.003)高于對(duì)照組(0.077±0.003),差異有統(tǒng)計(jì)學(xué)意義(P均0.05)；煙霧暴露12周組(0.492±0.003)及8周組(0.367±0.004)明顯高于4周組(0.220±0.005),差異有統(tǒng)計(jì)學(xué)意義(P均0.05)；煙霧暴露12周組(0.492±0.003)高于8周組(0.367±0.004),差異有統(tǒng)計(jì)學(xué)意義(P0.05)；NF-KBp65蛋白相對(duì)表達(dá)量在煙霧暴露4周組(0.330±0.003)、8周組(0.452±0.003)、12周組(0.596±0.003)高于對(duì)照組(0.186±0.001),差異有統(tǒng)計(jì)學(xué)意義(P均0.05)；煙霧暴露12周組(0.596±0.003)及8周組(0.452±0.003)高于4周組(0.330±0.003),差異有統(tǒng)計(jì)學(xué)意義(P均0.05)；煙霧暴露12周組(0.596±0.003)高于8周組(0.452±0.003),差異有統(tǒng)計(jì)學(xué)意義(P0.05)；③DGF-BB蛋白的表達(dá)與PDGF-BB mRNA的相對(duì)表達(dá)量及與NF-KBp65蛋白的表達(dá)均呈正相關(guān)(r=0.686、r=0.501,P值均0.01)。 結(jié)論：香煙煙霧暴露8周使大鼠肺動(dòng)脈壓力增高,形成肺動(dòng)脈高壓；香煙煙霧暴露4周大鼠肺組織中PDGF-BB表達(dá)增高,促使肺血管重塑,至12周漸增高,促使肺動(dòng)脈高壓形成；香煙煙霧暴露4至12周大鼠肺組織中NF-KBp65表達(dá)漸增高。煙霧暴露大鼠肺組織中PDGF-BB在轉(zhuǎn)錄和翻譯水平表達(dá)均增高,且PDGF-BB和NF-kB蛋白表達(dá)有相關(guān)性,提示PDGF-BB和NF-kB在煙霧暴露引起肺動(dòng)脈平均壓增高的過(guò)程中可能發(fā)揮了一定作用。
[Abstract]:Aim: to investigate the effects of smoke exposure on the expression of platelet derived growth factor-BB (PDGF-BB) and nuclear factor-kB (NF-kB) p65 in rat lung tissue, and to explore the mechanism of pulmonary hypertension induced by smoke exposure. Methods: Thirty-two male Wistar rats were randomly divided into control group (n = 8) and smoke exposure group (n = 8) for 12 weeks. Pulmonary hypertension model was established in smoke exposure group (n = 8). The rats in the smoke exposure group were put into the self-made experimental rats' passive smoking box for passive smoking. The smoke exposure group was exposed to smoke for 4 weeks for 12 weeks. The other conditions were the same in the control group except for no smoke exposure. After the rat model was established successfully, the mean pulmonary artery pressure (mean pulmonary arterial pressure, mPAP) was measured by right cardiac catheterization method. The intact free heart and lung tissues were obtained under aseptic condition. The right heart hypertrophy index (right ventricle hypertrophy index, RVHI) was calculated, and the left lung tissue was frozen in refrigerator at -80 鈩，

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