本文選題：肢體缺血預(yù)處理　切入點：胎兒缺氧/復(fù)氧損傷　出處：《福建醫(yī)科大學(xué)》2014年碩士論文

【摘要】：目的探索母體肢體缺血預(yù)處理（LIP）對宮內(nèi)窘迫胎鼠復(fù)氧后海馬神經(jīng)元線粒體結(jié)構(gòu)和功能的影響。 方法孕20天的SD大鼠麻醉后開腹采用微動脈夾鉗夾母鼠通向子宮和卵巢的動靜脈15min制備胎鼠宮內(nèi)窘迫模型；同時將孕鼠右下肢股動脈阻斷5min/再灌注5min，共3次循環(huán)進(jìn)行母體的LIP。將24只孕鼠隨機(jī)分為4組，每組6只：空白對照組（S組），LIP對照組，胎兒宮內(nèi)窘迫組（FD組），LIP+胎兒宮內(nèi)窘迫組。孕21天時剖宮取活胎鼠斷頭取腦，每只孕鼠取6只活胎鼠。通過電鏡下觀察胎鼠海馬CA1區(qū)線粒體超微結(jié)構(gòu)的變化；流式細(xì)胞儀檢測海馬線粒體跨膜電位、海馬組織活性氧（ROS）的變化；定磷法檢測海馬組織ATP含量變化；比色法測定Mn-SOD活性及MDA含量。 結(jié)果(1)與S組比較，LIP組電鏡下觀察胎鼠海馬CA1區(qū)線粒體結(jié)構(gòu)基本正常，無明顯變化。線粒體膜電位、活性氧含量、ATP含量、Mn-SOD活性及MDA含量無明顯變化（均P0.05）。（2）與S組比較，F(xiàn)D組電鏡下觀察胎鼠海馬CA1區(qū)線粒體呈高度腫脹、部分脊斷裂、消失，甚至呈空泡狀，線粒體數(shù)目減少。線粒體膜電位下降、活性氧含量增加、ATP含量下降、Mn-SOD活性降低、MDA含量增加（均P0.05）。（3）與S組相比，LIP+FD組胎鼠海馬CA1區(qū)線粒體呈輕度腫脹，部分脊斷裂，線粒體外膜完整，線粒體膜電位下降、活性氧含量增加、ATP含量下降、Mn-SOD活性降低、MDA含量增加（均P0.05）。（4）與FD組比較，LIP+FD組胎鼠海馬CA1區(qū)線粒體的超微結(jié)構(gòu)保持較好的完整性，腫脹度減輕，抑制了線粒體膜電位的降低，減少海馬ATP含量下降，Mn-SOD活性顯著增高，，MDA含量減少（均P0.05）。 結(jié)論母體肢體缺血預(yù)處理可抑制宮內(nèi)窘迫胎鼠復(fù)氧后海馬神經(jīng)元線粒體超微結(jié)構(gòu)的改變，減輕線粒體膜電位的下降，減少海馬組織ATP含量降幅，減少ROS生成，增強(qiáng)線粒體抗氧化能力，改善線粒體功能。
[Abstract]:Objective to investigate the effects of maternal limb ischemic preconditioning (LIP) on the mitochondrial structure and function of hippocampal neurons in fetal rats with intrauterine distress after reoxygenation. Methods Sprague-Dawley rats were anesthetized on the 20th day of gestation and intrauterine distress model was established by using arteriovenous 15min (15min) which was clamped by arteriovenous clamp to the uterus and ovary. At the same time, the femoral artery of the right lower extremity of pregnant rats was blocked by 5min/ reperfusion for 5 minutes, and the maternal lip was carried out 3 times. 24 pregnant rats were randomly divided into 4 groups, 6 rats in each group: the blank control group (S group) and the control group (group S). Fetal intrauterine distress group (FD group) and lip fetal distress group (FID group). At 21 days of gestation, the fetal rat head was cut off and the brain was taken from each pregnant rat. The ultrastructure of mitochondria in CA1 area of fetal rat hippocampus was observed by electron microscope. The changes of mitochondrial transmembrane potential and reactive oxygen species (Ros) in hippocampal tissue were detected by flow cytometry, ATP content in hippocampal tissue was detected by phosphorus determination method, Mn-SOD activity and MDA content in hippocampus were measured by colorimetric method. Results 1) compared with S group, the mitochondrial structure in the hippocampal CA1 area of fetal rats was basically normal, and the mitochondrial membrane potential was not changed under electron microscope in lip group. There was no significant change in the activity of Mn-SOD and the content of MDA (P0.05. 0. 0. 0. 0. 0. 0. 5%) compared with group S, the mitochondria in CA1 area of fetal rat hippocampus were highly swollen, some ridges were broken, disappeared, or even vacuolated under electron microscope in FD group. The number of mitochondria decreased, the mitochondrial membrane potential decreased, the content of reactive oxygen species increased, the content of ATP decreased, the activity of Mn-SOD decreased, the activity of Mn-SOD decreased and the content of MDA increased. Compared with group S, the mitochondria of CA1 area of fetal rats in lip FD group were slightly swollen and some ridges were broken. The mitochondrial outer membrane was intact, the mitochondrial membrane potential was decreased, the content of reactive oxygen species was increased, the activity of Mn-SOD was decreased, and the content of MDA was increased (P0.05, P < 0.05). Compared with the FD group, the ultrastructure of mitochondria in the CA1 area of fetal rats in the lip FD group maintained a better integrity than that in the FD group. The swelling degree was reduced, the decrease of mitochondrial membrane potential was inhibited, the content of ATP in hippocampus was decreased, the activity of Mn-SOD was increased significantly and the content of MDA was decreased (all P 0.05). Conclusion the maternal limb ischemic preconditioning can inhibit the changes of mitochondrial ultrastructure of hippocampal neurons after reoxygenation in fetal rats with intrauterine distress, reduce the decrease of mitochondrial membrane potential, decrease the content of ATP and decrease the production of ROS in hippocampus. Enhance the antioxidant capacity of mitochondria and improve the function of mitochondria.
【學(xué)位授予單位】：福建醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R614

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相關(guān)期刊論文 前2條

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本文編號：1695289