本文選題：硫化氫　切入點(diǎn)：腦缺血再灌注　出處：《南華大學(xué)》2014年碩士論文　論文類型：學(xué)位論文

【摘要】：目的：觀察外源性硫化氫（hydrogen sulfide, H2S）對(duì)大鼠局灶性腦缺血再灌注損傷的保護(hù)作用并探討其可能的機(jī)制。 方法：50只SD雄性大鼠隨機(jī)分為假手術(shù)組、缺血再灌注模型組、10μmol/kg、50μmol/kg和100μmol/kg外源性H2S供體硫氫化鈉（sodiumhydrosulfide, NaHS）處理組，，每組10只。采用線栓法建立SD雄性大鼠缺血再灌注損傷模型，缺血2小時(shí)再灌注72小時(shí)。NaHS（10、50和100μmol/kg）在再灌注前30分鐘腹腔注射；假手術(shù)組、缺血再灌注模型組給予等量生理鹽水腹腔注射。再灌注6h、12h、24h、48h、72h對(duì)各組進(jìn)行神經(jīng)功能缺損評(píng)分。再灌注72小時(shí)后處死大鼠，采用2,3,5-氯化三苯基四氮唑（2,3,5-three phenyl tetrazolium chloride, TTC）染色觀察并計(jì)算腦梗死的體積和比例。取缺血周邊腦組織用分光光度法檢測(cè)腦組織勻漿上清液中活性氧（reactive oxygen species, ROS）水平、丙二醛（malonaldehyde, MDA）含量和超氧化物歧化酶（superoxide dismutase, SOD）的活性；用雙抗體夾心法測(cè)定腦組織勻漿上清液中總抗氧化力（total antioxidant capacity, T-AOC）的水平；用ELISA法測(cè)定腦組織勻漿上清液中還原型谷胱甘肽（reduced glutathione hormon,GSH）的水平。用PCR和Western blot檢測(cè)缺血周邊腦組織中腦源性神經(jīng)營(yíng)養(yǎng)因子（brain derived neurotrophic factor, BDNF）和酪氨酸激酶B（tyrosine kinase B,TrkB）mRNA和蛋白的表達(dá)。 結(jié)果： 1、與缺血再灌注損傷模型組比較， NaHS（50和100μmol/Kg）處理組大鼠神經(jīng)功能缺損明顯改善，肌力明顯增強(qiáng)，神經(jīng)功能評(píng)分顯著性降低（均P0.05）。 2、與假手術(shù)組比較，缺血再灌注損傷組大鼠缺血周邊區(qū)腦組織中H2S濃度顯著降低（P＜0.05），NaHS（50和100μmol/Kg）處理組大鼠缺血周邊區(qū)腦組織中H2S濃度與模型組比較均顯著升高，呈現(xiàn)劑量依賴性（均P0.05）。 3、與缺血再灌注損傷模型組比較，NaHS（50和100μmol/Kg）處理組的鼠腦梗死體積和比例顯著降低，呈現(xiàn)劑量依賴性（均P0.05）。 4、與缺血再灌注損傷模型組比較，NaHS（50和100μmol/Kg）處理組大鼠缺血周邊腦組織勻漿上清液中ROS水平和MDA含量顯著降低（均P＜0.05），缺血周邊腦組織勻漿上清液中T-AOC水平、SOD的活性和GSH水平顯著增加（均P＜0.05）。 5、與缺血再灌注損傷模型組比較，NaHS（50和100μmol/Kg）處理組大鼠缺血周邊腦組織中BDNF和TrkB的表達(dá)顯著增加（均P㩳0.05）。 結(jié)論：外源性H2S對(duì)腦缺血再灌注損傷具有保護(hù)作用，其機(jī)制可能與外源性H2S抑制氧化應(yīng)激、上調(diào)BDNF和TrkB的表達(dá)有關(guān)。
[Abstract]:Aim: to observe the protective effect of exogenous hydrogen sulfide hydrogen sulfide (H _ 2S) on focal cerebral ischemia-reperfusion injury in rats and to explore its possible mechanism. Methods Fifty Sprague-Dawley male rats were randomly divided into sham-operation group, ischemia reperfusion model group (10 渭 mol / kg ~ (50) mol/kg) and exogenous H _ 2S donor sodium sulfide (NaHS) treatment group (n = 10). After 2 hours of ischemia and 72 hours of reperfusion, 50 and 100 渭 mol / kg NaHSN were injected intraperitoneally 30 minutes before reperfusion. The rats in the ischemia reperfusion model group were given intraperitoneal injection of the same amount of normal saline. The neurological impairment scores were evaluated in each group at 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion. After 72 hours of reperfusion, the rats were killed. The volume and proportion of cerebral infarction were observed and calculated by TTC staining. The level of reactive oxygen species (Ros) in the supernatant of brain homogenate was detected by spectrophotometric method, and the content of reactive oxygen species (ROSs) in the supernatant of brain homogenate was determined by spectrophotometry. The content of malondialdehyde malonaldehydeand the activity of superoxide dismutase (SOD) were determined by double antibody sandwich method. The level of reduced glutathione reduced glutathione hormonium (GSH) in the supernatant of brain tissue homogenate was determined by ELISA method, and the expression of brain-derived neurotrophic factor (BDNFF) and tyrosine kinase (kinase) TrkBN mRNA and protein in peripheral ischemic brain tissue were detected by PCR and Western blot. Results:. 1.Compared with the model group of ischemia-reperfusion injury, NaHS(50 and 100 渭 mol / kg group significantly improved the nerve function defect, enhanced the muscle strength, and significantly decreased the neurological function score (all P 0.05). 2. Compared with the sham operation group, the concentration of H2S in the cerebral tissue of the ischemic peripheral area of rats in the ischemia-reperfusion group decreased significantly (P < 0.05), and the concentration of H _ 2S in the brain tissue of the ischemic peripheral area of the rats in the treatment group was significantly higher than that in the model group (P < 0.05), and the concentration of H _ 2S in the brain tissue of the ischemic peripheral area was significantly higher than that in the model group (all P < 0.05). 3Compared with the model group of ischemia-reperfusion injury, the volume and proportion of cerebral infarction in the NaHS 50 and 100 渭 mol / kg groups were significantly decreased in a dose-dependent manner (all P 0.05). 4. Compared with the model group of ischemia-reperfusion injury, the level of ROS and the content of MDA in the supernatant of cerebral homogenate of rats treated with NaHS 50 and 100 渭 mol / kg significantly decreased (all P < 0.05), the activity of T-AOC and the activity of T-AOC in the supernatant of cerebral homogenate of ischemic peripheral brain tissue decreased significantly (P < 0.05). The level of GSH increased significantly (all P < 0.05). 5. Compared with the model group of ischemia reperfusion injury, the expression of BDNF and TrkB in the ischemic peripheral brain tissue of rats treated with NaHS 50 and 100 渭 mol / kg were significantly increased (all P? 0.05. Conclusion: exogenous H2S has protective effect on cerebral ischemia-reperfusion injury, and its mechanism may be related to the inhibition of oxidative stress and up-regulation of BDNF and TrkB expression by exogenous H2S.
【學(xué)位授予單位】：南華大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R743.3

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