本文關(guān)鍵詞： 鹽酸吸入 急性肺損傷 雷公藤紅素　出處：《青島大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

【摘要】：目的:圍術(shù)期急性肺損傷/急性呼吸窘迫綜合癥是臨床常見的肺部并發(fā)癥,胃內(nèi)容物誤吸是其中的主要原因之一。對(duì)于此類急性肺損傷,目前主要是通過(guò)給氧、機(jī)械通氣等呼吸支持措施治療以及糖皮質(zhì)激素藥物治療,然而療效均不滿意。本研究試圖通過(guò)觀察預(yù)先使用藥物雷公藤紅素對(duì)鹽酸吸入性肺損傷是否具有保護(hù)作用,以其為臨床治療提供理論依據(jù),進(jìn)而探討雷公藤紅素對(duì)小鼠鹽酸吸入性急性肺損傷的保護(hù)機(jī)制。方法:將24只健康清潔級(jí)小鼠按隨機(jī)數(shù)字表法分成4組(n=6):A組,正常對(duì)照組;B組,雷公藤紅素腹腔給藥組;C組,鹽酸吸入性急性肺損傷組;D組:鹽酸吸入性急性肺損傷+雷公藤紅素腹腔給藥組。四組小鼠預(yù)先連續(xù)3天腹腔注射藥物處理:A組和C組每天用3ml/kg生理鹽水腹腔內(nèi)注射,B組和D組用雷公藤紅素3mg/kg(約為3ml/kg)腹腔注射,每天一次。實(shí)驗(yàn)開始時(shí)四組小鼠禁食12h但不禁水,用戊巴比妥鈉(50mg/kg)腹腔注射麻醉,用24號(hào)套管針的外套管進(jìn)行氣管插管,操作成功后C組和D組氣管內(nèi)先注射鹽酸(PH=1.5,2ml/kg),然后注入少許空氣使藥液完全進(jìn)入肺內(nèi)制作小鼠肺損傷模型;A組和B組注射等量生理鹽水和空氣。然后拔除氣管插管由小鼠自主呼吸空氣,并允許小鼠自由接觸水和食物。采用氣管內(nèi)滴注鹽酸的方法制備小鼠吸入性急性肺損傷模型。于滴注后6 h時(shí)處死小鼠取肺組織,觀察小鼠鹽酸吸入6 h后肺組織病理切片,測(cè)定肺組織勻漿中超氧化物岐化酶(SOD)活力與丙二醛(MDA)含量,并檢測(cè)肺組織中腫瘤壞死因子-α(TNF-α)和白介素-6(IL-6)含量的變化以及巨噬細(xì)胞移動(dòng)抑制因子(MIF)和髓過(guò)氧化物酶(MPO)的改變。結(jié)果:1、肺組織病理學(xué)結(jié)果顯示:與C組相比,D組肺組織結(jié)構(gòu)清晰,肺間質(zhì)腫脹、炎性細(xì)胞浸潤(rùn)及出血明顯減輕。2、與A組相比,C組、D組MDA值升高(P0.01),SOD活力降低(P0.01),且C組MDA值比D組高(P0.01),SOD活力比D組低(P0.01)。3、TNF-α、IL-6含量均以A組和B組為低,C組為最高,D組居中。與A組相比,C組、D組TNF-α值、IL-6值均升高(P0.01),且C組TNF-α值、IL-6值均高于D組(P0.01)/4、MIF、MPO含量以A組和B組為低,C組為最高,D組居中。與A組相比,C組、D組MIF值、MPO值均升高(P0.01),且C組MIF值、MPO值均高于D組(P0.01)。結(jié)論:1.鹽酸吸入可引起肺彌漫性急性損傷,表現(xiàn)為呼吸急促、氧分壓下降,肺組織病理改變。2.鹽酸吸入導(dǎo)致的急性肺損傷/急性呼吸窘迫綜合征通過(guò)促進(jìn)肺組織的脂質(zhì)過(guò)氧化反應(yīng),破壞氧化-抗氧化平衡以及產(chǎn)生大量炎癥因子TNF-a、IL-6而造成。3.雷公藤紅素對(duì)小鼠鹽酸吸入性急性呼吸窘迫綜合征有保護(hù)作用,其機(jī)制可能與其抑制肺組織炎癥因子TNF-a、IL-6的產(chǎn)生和釋放,抑制脂質(zhì)過(guò)氧化反應(yīng),提高抗氧化能力、以及抑制肺組織MIF表達(dá)、減少中性粒細(xì)胞浸潤(rùn)有關(guān)。
[Abstract]:Objective: perioperative acute lung injury / acute respiratory distress syndrome (ARDS) is a common pulmonary complication, and gastric misprision is one of the main causes. Respiratory support measures such as mechanical ventilation and glucocorticoid therapy. However, the curative effect is not satisfactory. This study attempts to observe the protective effect of tripterygium tripterygium on inhaled hydrochloric acid lung injury in order to provide theoretical basis for clinical treatment. To explore the protective mechanism of tripterygium wilfordii on acute lung injury induced by hydrochloric acid inhalation in mice methods: 24 healthy and clean grade mice were randomly divided into 4 groups (n = 4) and normal control group (n = 6: a). Group B, Tripterygium wilfordii intraperitoneal administration group; Group C: acute lung injury induced by hydrochloric acid inhalation; Group D: Tripterygium wilfordii was administered intraperitoneally with hydrochloric acid inhaled acute lung injury. Four groups of mice were intraperitoneally injected with 3 ml / kg physiological saline for 3 ml / kg per day for 3 consecutive days. Group B and group D were intraperitoneally injected with tripterine 3 mg / kg (about 3 ml / kg) once a day. At the beginning of the experiment, the mice of the four groups fasted for 12 hours but could not help drinking water. 50 mg / kg pentobarbital sodium was used intraperitoneally to anesthetize and endotracheal intubation was performed with the outer tube of cannula 24. After successful operation, PH1.5 hydrochloride was injected into the trachea of group C and group D. Then a little air was injected into the lung to make the model of lung injury in mice. Group A and group B were injected with the same amount of saline and air. Then tracheal intubation was pulled out and the air was breathed autonomously by the mice. Mice were given free access to water and food. The model of acute lung injury was established by intratracheal instillation of hydrochloric acid. The mice were killed at 6 h after infusion. The pathological sections of lung tissue were observed after inhalation of hydrochloric acid for 6 h, and the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in the homogenate of lung tissue were determined. The changes of tumor necrosis factor- 偽 (TNF- 偽) and interleukin-6 (IL-6) in lung tissue and the changes of macrophage migration inhibitory factor (MIF) and myeloperoxidase (MPO) were also detected. Change. Result: 1. The results of lung histopathology showed that compared with group C, lung tissue structure was clear, interstitial swelling, inflammatory cell infiltration and hemorrhage were significantly alleviated in group D, and group C was significantly less than group A. The activity of MDA in group D was higher than that in group D, and the activity of MDA in group C was higher than that in group D, and the activity of MDA in group C was lower than that in group D. The content of TNF- 偽 IL-6 in group A and group B was the highest in group C, and the TNF- 偽 value in group D was higher than that in group A (P 0.01). Moreover, the level of TNF- 偽 and IL-6 in group C was higher than that in group D (P 0.01 / 4). The MPO content in group A and group B was the highest in group C, and the highest in group D, and in comparison with group A, group C was higher than that in group A. The MIF value of group D was higher than that of group D (P 0.01), and the value of MIF in group C was higher than that of group D (P 0.01). Conclusion: 1. Inhaled hydrochloric acid can induce diffuse acute lung injury. Acute lung injury / acute respiratory distress syndrome induced by inhalation of hydrochloric acid promotes lipid peroxidation in lung tissue. Tripterygium tripterygium has protective effect on acute respiratory distress syndrome induced by hydrochloric acid. The mechanism may be related to the inhibition of the production and release of TNF-a IL-6, the inhibition of lipid peroxidation, the enhancement of antioxidant capacity, and the inhibition of MIF expression in lung tissue. The decrease of neutrophil infiltration is related to.
【學(xué)位授予單位】：青島大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R614

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