本文選題：煙霧吸入性損傷 + 依達拉奉��； 參考：《天津醫(yī)科大學》2013年碩士論文

【摘要】：研究背景： 吸入性損傷是由煙霧和(或)熱力引起的肺實質和呼吸道的聯(lián)合損傷,是燒傷患者早期死亡的主要原因之一。因其發(fā)病機制與某些炎癥因子密切相關,可引起全身炎癥反應綜合征,繼發(fā)其他臟器損傷,所以其在臨床治療上依然是一個難題。依達拉奉是一種新型強效的抗氧化劑,在抗炎癥因子和清除氧自由基過程中發(fā)揮重要作用,本研究通過應用依達拉奉干預吸入性損傷的病理生理過程,觀察其對肺功能的保護作用。 研究目的： 1.通過檢測大鼠血清白細胞介素-6(IL-6)、白細胞介素-10(IL-10)、腫瘤壞死因子-α(TNF-α)含量水平,探討依達拉奉對煙霧吸入性損傷早期炎癥介質的影響。 2.通過檢測大鼠肺組織勻漿中丙二醛(MDA)含量、髓過氧化物酶(MPO)和超氧化物歧化酶(SOD)活性水平,探討依達拉奉對煙霧吸入性損傷早期氧化/抗氧化因子的影響。 3.本研究通過觀察依達拉奉對煙霧吸入性損傷后大鼠炎癥介質以及氧化／抗氧化平衡的影響,探討依達拉奉對早期煙霧吸入性損傷的肺保護作用及機制,為臨床治療吸入性損傷提供新思路。 研究方法： 將32只雄性Sprague-Dawle大鼠采用隨機數(shù)字表法隨機分為4組,每組8只。分別為正常對照組(A組),致傷空白組(B組),致傷依達拉奉治療組(C組),致傷依達拉奉預防組(D組)。A組無處理,B組、C組、D組建立吸入性損傷模型。D組致傷前l(fā)Omin給予腹腔注射依達拉奉(9mg·kg-1),C組致傷后30min給予腹腔注射依達拉奉(9mg·kg-1),B組致傷后30min給予等量生理鹽水。傷后6小時留取各組大鼠股動脈血液樣本5ml離心取血清檢測腫瘤壞死因子-α(TNF-α)、白細胞介素-6(IL-6)、白細胞介素-10(IL-10)含量,留取肺組織制備肺組織勻漿后測定丙二醛(MDA)含量、超氧化物歧化酶(SOD)和肺髓過氧化物酶(MPO)活性。取部分右肺組織經(jīng)4%甲醛溶液固定后做病理HE染色切片光鏡觀察。 結果： 1.一般情況觀察及標本大體觀察：一般情況：使用隨機數(shù)字表法隨機分組,各組間大鼠體重比較無統(tǒng)計學意義,所有致傷動物在致傷過程中無一例死亡,大鼠致傷后均出現(xiàn)呼吸急促,聽診肺部出現(xiàn)哮鳴音,心率加快,煩躁不安,放置室內空氣流通地5-10分鐘后上述癥狀逐漸消失。而空白對照組無呼吸急促及煩躁不安。活殺大鼠后取標本大體觀察：空白對照組(A組)大鼠肺組織大致呈淡紅色,無充血水腫；致傷空白組(B組)大鼠組織呈暗紅色,明顯充血水腫,部分肺組織有淤血；致傷依達拉奉治療組(C組)大鼠肺組織部分充血水腫,有瘀斑；致傷依達拉奉預防組(D組)大鼠肺組織充血明顯減輕,僅有少量出血點。 2.肺組織HE病理切片觀察：光鏡下空白對照組(A組)肺泡結構完整,肺泡壁均勻一致,肺泡腔少許滲液,無紅白細胞滲出；致傷空白組(B組)肺泡間隔明顯不均勻,肺間隔可見大量中性粒細胞浸潤；致傷依達拉奉治療組(C組)肺泡間隔中性粒細胞浸潤減輕,肺泡間隔稍均勻；致傷依達拉奉預防組(D組)肺泡結構較清晰,肺泡間隔少量中性粒細胞浸潤。 3.各組大鼠血清TNF-α,IL-6及IL-10的比較：與致傷空白組(B組)相比,致傷依達拉奉治療組(C組)TNF-α、IL-6顯著降低(P0.01),IL-10水平顯著升高(P0.05),致傷依達拉奉預防組(D組)上述變化更明顯(P0.01)。 4.各組大鼠肺組織勻漿MPO、MDA、SOD的比較：與致傷空白組(B組)相比,致傷依達拉奉治療組(C組)MPO、MDA顯著降低(P0.01),SOD水平顯著升高(P0.05),致傷依達拉奉預防組(D組)上述變化更明顯(P0.01)。 結論： 1.吸入性損傷后,肺組織明顯充血水腫,肺泡結構破壞,肺泡間隔極不均勻,大量炎性細胞浸潤。依達拉奉治療組和預防組可以使上述損傷減輕,且預防組損傷減輕程度更加明顯。 2.依達拉奉可能通過抗氧化和抑制炎癥介質的作用對煙霧吸入性損傷后肺臟發(fā)揮保護作用,且預防性用藥效果較好。
[Abstract]:Research background:
Inhalation injury is a joint injury of lung parenchyma and respiratory tract caused by smoke and / or heat. It is one of the main causes of early death in burn patients. Because its pathogenesis is closely related to some inflammatory factors, it can cause systemic inflammatory response syndrome and secondary organ damage, so it is still a difficult problem in clinical treatment. Edaravone is a new potent antioxidants, play an important role in anti-inflammatory cytokines and oxygen free radical scavenging process, this study through the application of edaravone inhalation pathophysiological process of the injury, to observe the protective effect on lung function.
The purpose of the study is:
1. through the detection of serum interleukin -6 (IL-6), interleukin -10 (IL-10), tumor necrosis factor alpha (TNF- alpha) levels, to investigate the effect of edaravone early inflammatory mediators on smoke inhalation injury.
2. through the detection of rat lung tissue homogenate malondialdehyde (MDA) content, myeloperoxidase (MPO) and superoxide dismutase (SOD) activity level, to explore the effect of inhalation injury of edaravone oxidant / antioxidant factor on the smoke.
3. by observing the effects of edaravone on the inflammatory mediators and oxidation / antioxidant balance in rats after smoke inhalation injury, the protective effects and mechanisms of edaravone on early smoke inhalation injury were explored to provide a new idea for clinical treatment of inhalation injury.
Research methods:
32 male Sprague-Dawle rats were randomly divided into 4 groups, 8 rats in each group, which were the normal control group (group A), the injury blank group (group B), the injured edaravone group (group C), the injured edaravone prevention group (D group).A group no treatment, B group, C group, and D group to establish the.D group before injuring lOmin intraperitoneal injection. Edaravone (9mg. Kg-1), group C was injected with edaravone (9mg. Kg-1) intraperitoneally after injury in group C, and 30min was given equal amount of physiological saline after injury in group B. 6 hours after injury, the blood samples of femoral artery in each group were left to take the blood samples from the femoral artery to detect tumor necrosis factor - alpha (TNF- a), -6 (IL-6), interleukin content and lung. Determination of content of tissue preparation of lung tissue homogenate (MDA) content, superoxide dismutase (SOD) and myeloperoxidase (MPO) activity. The right lung tissue by Formaldehyde Solution in 4% after being fixed under light microscope HE staining.
Result錛，

本文編號：2047915