本文選題：阻塞性睡眠呼吸暫停低通氣綜合征 + 間歇缺氧　； 參考：《蘭州大學(xué)》2014年碩士論文

【摘要】：目的通過(guò)模擬阻塞性睡眠呼吸暫停低通氣綜合征(OSAHS)患者睡眠過(guò)程中反復(fù)發(fā)生的間歇低氧／再氧合過(guò)程,建立間歇缺氧模型,探討間歇缺氧大鼠體內(nèi)氧化應(yīng)激、炎癥反應(yīng)的機(jī)制。 方法將16只雄性SD大鼠進(jìn)行稱重后,隨機(jī)分為兩組,間歇缺氧(IH)組和對(duì)照(NC)組,每組8只,將其放入間歇缺氧模擬艙內(nèi),向艙內(nèi)循環(huán)充入氮?dú)狻⒀鯕夂蛪嚎s空氣,循環(huán)周期為120s,輸入純氮?dú)?0秒(模擬艙中氧濃度逐漸下降至6-7%),靜息10秒(模擬艙中氧濃度維持在6-7%),輸入純氧氣20秒(模擬艙中氧濃度逐漸上升至20-21%),輸入壓縮空氣60秒(模擬艙中氧濃度波動(dòng)在20.8±0.3%)。實(shí)驗(yàn)時(shí)間設(shè)計(jì)為每天8小時(shí)(9am-17pm),每周7天,持續(xù)4周,共28天。將對(duì)照組大鼠于每天相同時(shí)間置于相同規(guī)格的動(dòng)物飼養(yǎng)艙內(nèi),并通入相同流量的空氣。第29天處死大鼠后,用生化法測(cè)定大鼠血清MDA. SOD.GSH-PX水平,用放免法測(cè)定大鼠血清IL-6和TNF-a水平。 結(jié)果1.血清MDA水平：正常對(duì)照組為5.09±0.51nmol/ml,IH組為5.74±0.38nmol/ml。與對(duì)照組比較,IH組大鼠血清MDA水平升高,且具有統(tǒng)計(jì)學(xué)差異(P=0.0110.05)。2.血清SOD水平：正常對(duì)照組為67.21±6.68U/ml,IH組56.70±6.34U/ml。與對(duì)照組相比,IH組大鼠血請(qǐng)SOD水平降低,且具有統(tǒng)計(jì)學(xué)差異(P=0.006＜0.05)。3.血清GSH-PX水平：正常對(duì)照組為811.50±14.90U/ml,IH組779.16±30.27U/ml。與對(duì)照組相比,IH組大鼠血清GSH-PX水平降低,且具有統(tǒng)計(jì)學(xué)差異(P=0.017＜0.05)。4.血清IL-6水平：正常對(duì)照組為166.04±30.92pg/ml,IH組為211.01±33.24pg/ml.與對(duì)照組比較,IH組大鼠血清IL-6水平升高,且具有統(tǒng)計(jì)學(xué)差異(P=0.014＜0.05)。4.血清TNF-a水平：正常對(duì)照組為59.11±10.07pg/ml,IH組74.22±7.68pg/ml.與對(duì)照組相比,IH組大鼠血請(qǐng)TNF-a水平升高,且具有統(tǒng)計(jì)學(xué)差異(P=0.005＜0.05)。 結(jié)論1.間歇缺氧條件下能導(dǎo)致大鼠血清MDA水平升高,而血清SOD和GSH水平降低,提示間歇缺氧大鼠體內(nèi)存在氧化應(yīng)激狀態(tài),間歇缺氧可以導(dǎo)致大鼠體內(nèi)抗氧化能力的下降；2.間歇缺氧條件下能導(dǎo)致大鼠血清TNF-a和IL-6水平升高,提示間歇缺氧大鼠體內(nèi)存在炎癥反應(yīng)。 目的通過(guò)模擬阻塞性睡眠呼吸暫停低通氣綜合征(OSAHS)患者睡眠過(guò)程中反復(fù)發(fā)生的間歇低氧／再氧合過(guò)程,建立間歇缺氧模型,探討間歇缺氧對(duì)大鼠甲狀腺激素、甲狀腺超微結(jié)構(gòu)及對(duì)大鼠甲狀腺Peroxiredoxin5表達(dá)的影響。 方法將16只雄性SD大鼠進(jìn)行稱重后,隨機(jī)分為兩組,間歇缺氧(IH)組和對(duì)照(NC)組,每組8只,將其放入間歇缺氧模擬艙內(nèi),向艙內(nèi)循環(huán)充入氮?dú)�、氧氣和壓縮空氣,循環(huán)周期為120s,輸入純氮?dú)?0秒(模擬艙中氧濃度逐漸下降至6-7%),靜息10秒(模擬艙中氧濃度維持在6-7%),輸入純氧氣20秒(模擬艙中氧濃度逐漸上升至20-21%),輸入壓縮空氣60秒(模擬艙中氧濃度波動(dòng)在20.8±0.3%)。實(shí)驗(yàn)時(shí)間設(shè)計(jì)為每天8小時(shí)(9am-17pm),每周7天,持續(xù)4周,共28天。將對(duì)照組大鼠于每天相同時(shí)間置于相同規(guī)格的動(dòng)物飼養(yǎng)艙內(nèi),并通入相同流量的空氣。第29天處死大鼠后,用放免法測(cè)定大鼠血清FT3、FT4、TSH水平,于電鏡下觀察大鼠甲狀腺超微結(jié)構(gòu)的改變,用免疫組化方法測(cè)定大鼠甲狀腺中Peroxiredoxin5表達(dá)。 結(jié)果1.血清FT3水平：正常對(duì)照組為0.40±0.17ng/dl,IH組為0.46±0.19ng/dl。與對(duì)照組比較,IH組大鼠血清FT3水平升高,但不具有統(tǒng)計(jì)學(xué)差異(P=0.5210.05)。2.血清FT4水平：正常對(duì)照組為4.20±0.92ng/dl,IH組2.98±0.64ng/dl。與對(duì)照組相比,IH組大鼠血清FT4水平降低,且具有統(tǒng)計(jì)學(xué)差異(P=0.0090.05)。3.血清TSH水平：正常對(duì)照組為12.34±1.89uIU/ml,IH組9.36±1.17uIU/ml。與對(duì)照組相比,IH組大鼠血清TSH水平降低,且具有統(tǒng)計(jì)學(xué)差異(P=0.0030.05)。4.IH組大鼠甲狀腺超微結(jié)構(gòu)：整體表現(xiàn)為缺氧改變。5.甲狀腺PRDX5的陽(yáng)性染色主要位于甲狀腺細(xì)胞的胞漿中,大鼠甲狀腺Peroxiredoxin5表達(dá)：正常對(duì)照組的平均光密度為0.22±0.01,CIH組的平均光密度為0.30±0.01。與對(duì)照組比較,IH組大鼠甲狀腺Peroxiredoxin5表達(dá)升高且差異具有統(tǒng)計(jì)學(xué)意義(P=0.0020.05)。 結(jié)論1.間歇缺氧條件下能導(dǎo)致大鼠血清FT4、TSH降低,提示了間歇缺氧可以引起大鼠下丘腦-垂體-甲狀腺軸及甲狀腺本身功能的下降或異常,從而導(dǎo)致甲狀腺激素水平發(fā)生改變；2.間歇缺氧條件下能導(dǎo)致大鼠甲狀腺超微結(jié)構(gòu)發(fā)生缺氧改變；3.間歇缺氧條件下能導(dǎo)致大鼠甲狀腺中PRDX5陽(yáng)性表達(dá)升高,提示了間歇缺氧可使大鼠甲狀腺抗氧化能力增加,間接提示了間歇缺氧大鼠甲狀腺存在氧化應(yīng)激狀態(tài)。
[Abstract]:Objective to simulate intermittent hypoxia / reoxygenation during the sleep process of patients with obstructive sleep apnea hypopnea syndrome (OSAHS), to establish an intermittent hypoxia model, and to explore the mechanism of oxidative stress and inflammation in intermittent hypoxia rats.
Methods 16 male SD rats were weighed. They were randomly divided into two groups, intermittent hypoxia (IH) group and control (NC) group, 8 in each group. They were put into the intermittent hypoxia simulated cabin and filled the cabin with nitrogen, oxygen and compressed air, the cycle period was 120s, and the pure nitrogen gas was entered for 30 seconds (the oxygen concentration in the simulated cabin gradually dropped to 6-7%) and resting for 10 seconds (simulation). The oxygen concentration in the cabin was maintained at 6-7%), the pure oxygen was input for 20 seconds (the oxygen concentration in the simulated cabin was gradually increased to 20-21%), and the compressed air was input for 60 seconds (the oxygen concentration in the simulated cabin was 20.8 + 0.3%). The experimental time was designed to be 8 hours a day (9am-17pm), 7 days a week, and 4 weeks for 28 days. The control group was placed in the same specification at the same time of the day. The animals were fed with the same flow of air. After twenty-ninth days of death, the rat serum MDA. SOD.GSH-PX level was measured by biochemical method, and the serum levels of IL-6 and TNF-a were measured by radioimmunoassay.
Results 1. serum MDA level: the normal control group was 5.09 + 0.51nmol/ml, and the IH group was 5.74 + 0.38nmol/ml. compared with the control group. The serum MDA level of the IH group was higher, and the serum SOD level of.2. was statistically different (P=0.0110.05).2. serum SOD level: the normal control group was 67.21 + 6.68U/ml, and the IH group 56.70 + 6.34U/ml. was compared with the control group. Decrease, and have statistical difference (P=0.006 < 0.05).3. serum GSH-PX level: normal control group was 811.50 + 14.90U/ml, IH group 779.16 + 30.27U/ml. compared with control group, IH group rats serum GSH-PX level decreased, and there was statistical difference (P=0.017 < 0.05).4. serum IL-6 level: normal control group was 166.04 + 30.92pg/ml, 211.01 group was 211.01 Compared with the control group, the serum IL-6 level of the rats in the IH group was increased, and the serum TNF-a level of.4. was statistically different (P=0.014 < 0.05).4. serum TNF-a level: the normal control group was 59.11 + 10.07pg/ml, and the IH group was 74.22 + 7.68pg/ml. compared with the control group, the TNF-a level of the IH group was higher, and there was a statistical difference (P=0.005 < 0.05).
Conclusion 1. intermittent hypoxia can lead to the increase of serum MDA level in rats, and the decrease of serum SOD and GSH levels, suggesting that there is oxidative stress in rats with intermittent hypoxia. Intermittent hypoxia can lead to the decrease of antioxidant capacity in rats. 2. intermittent hypoxia can lead to the increase of serum level of TNF-a and IL-6 in rats, suggesting intermittent deficiency. There are inflammatory reactions in the rats.
Objective to simulate intermittent hypoxia / reoxygenation during the sleep process of obstructive sleep apnea hypopnea syndrome (OSAHS), and to establish an intermittent hypoxia model to explore the effect of intermittent hypoxia on thyroid hormone, thyroid ultrastructure and the expression of thyroid gland Peroxiredoxin5 in rats.
Methods 16 male SD rats were weighed. They were randomly divided into two groups, intermittent hypoxia (IH) group and control (NC) group, 8 in each group. They were put into the intermittent hypoxia simulated cabin and filled the cabin with nitrogen, oxygen and compressed air, the cycle period was 120s, and the pure nitrogen gas was entered for 30 seconds (the oxygen concentration in the simulated cabin gradually dropped to 6-7%) and resting for 10 seconds (simulation). The oxygen concentration in the cabin was maintained at 6-7%), the pure oxygen was input for 20 seconds (the oxygen concentration in the simulated cabin was gradually increased to 20-21%), and the compressed air was input for 60 seconds (the oxygen concentration in the simulated cabin was 20.8 + 0.3%). The experimental time was designed to be 8 hours a day (9am-17pm), 7 days a week, and 4 weeks for 28 days. The control group was placed in the same specification at the same time of the day. The animals were fed with the same flow of air. After twenty-ninth days of death, the rat serum FT3, FT4, TSH levels were measured by radioimmunoassay. The ultrastructural changes of the thyroid gland were observed under the electron microscope, and the expression of Peroxiredoxin5 in the thyroid gland was measured by immunohistochemistry.
Results 1. serum FT3 level: the normal control group was 0.40 + 0.17ng/dl, and the IH group was 0.46 + 0.19ng/dl. compared with the control group. The serum FT3 level of the IH group was higher, but there was no statistical difference (P=0.5210.05).2. serum FT4 level: the normal control group was 4.20 + 0.92ng/dl, and the IH group 2.98 + 0.64ng/dl. was compared with the control group. Decrease, and have statistical difference (P=0.0090.05).3. serum TSH level: the normal control group was 12.34 + 1.89uIU/ml, the IH group 9.36 + 1.17uIU/ml. and the control group compared with the control group, the serum TSH level of the IH group decreased, and there was statistical difference (P=0.0030.05).4.IH group rat thyroid ultrastructure: the overall performance was the hypoxia to change.5. thyroid PRDX5. The positive staining was mainly located in the cytoplasm of thyroid cells. The expression of Peroxiredoxin5 in the thyroid gland was 0.22 + 0.01 in the normal control group, and the average light density in the CIH group was 0.30 + 0.01. compared with the control group. The thyroid Peroxiredoxin5 expression in the IH group was higher and the difference was statistically significant (P=0.0020.05).
Conclusion 1. intermittent hypoxia can lead to the decrease of FT4 and TSH in rat serum, suggesting that intermittent hypoxia can cause the decrease or abnormal function of hypothalamus pituitary thyroid axis and thyroid itself, which leads to the change of thyroid hormone level, and 2. intermittent hypoxia can lead to hypoxic ultrastructural anoxia in rats. 3. intermittent hypoxia can lead to the increase of PRDX5 positive expression in the thyroid gland of rats, suggesting that intermittent hypoxia can increase the antioxidant capacity of thyroid in rats and indirectly suggest that there is oxidative stress in the thyroid gland of rats with intermittent hypoxia.
【學(xué)位授予單位】：蘭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R766

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本文編號(hào)：1981780