本文選題：褪黑素 + 膽紅素腦病��； 參考：《桂林醫(yī)學院》2012年碩士論文

【摘要】：目的：探討褪黑素(melatonin, MT)對新生鼠膽紅素腦損傷的保護作用及其機制。方法：取SPF級5日齡SD大鼠90只,雌雄不限,完全隨機分為3組：生理鹽水對照組、膽紅素腦病模型組、MT治療組。MT治療組在制作膽紅素腦病動物模型基礎(chǔ)上給予MT治療,各組用免疫組化法檢測腦海馬組織BAX、BCL-2蛋白的表達變化,酶聯(lián)免疫吸附法檢測血清中神經(jīng)元特異性烯醇化酶(NSE)的水平,水迷宮實驗測試學習記憶能力。結(jié)果：MT治療組海馬神經(jīng)細胞在各時間點,海馬組織BAX陽性細胞率低于模型組(P0.05),高于對照組(P0.05);BCL-2陽性細胞各組均高于模型組(P0.05)高于對照組(P0.05);血清NSE水平均低于模型組(P0.05),高于對照組(P0.05);水迷宮實驗：褪黑素治療組在各時間點找到安全平臺的潛伏期均明顯短于模型組(P0.05),穿越平臺次數(shù)較模型組明顯增多,兩組均低于對照組。結(jié)論：新生大鼠膽紅素腦損傷后給予褪黑素干預(yù),可以提高腦組織的bcl-2的表達,抑制bax的表達,降低NSE的表達,發(fā)揮神經(jīng)保護作用,可以改善膽紅素相關(guān)性腦損傷所致的學習記憶障礙。
[Abstract]:Aim: to investigate the protective effect of melatonin (MTL) on bilirubin brain injury in neonatal rats and its mechanism. Methods: ninety male and female SD rats of SPF grade 5 days old were randomly divided into 3 groups: saline control group, bilirubin encephalopathy model group, MT treatment group, and MT treatment group on the basis of making bilirubin encephalopathy animal model. The expression of BCL-2 protein in brain tissue was detected by immunohistochemistry, the level of neuron-specific enolase (NSE) in serum was detected by enzyme-linked immunosorbent assay (Elisa), and the ability of learning and memory was tested by water maze test. Results the hippocampal neurons in the treatment group were at different time points. The rate of BAX positive cells in hippocampal tissue was lower than that in the model group and higher than that in the control group (P 0.05). The serum NSE level was lower than that in the model group and higher than that in the control group (P 0.05). The water maze test showed that melatonin was treated with melatonin. The latency of finding safe platform at each time point in the group was significantly shorter than that in the model group (P 0.05), and the number of crossing the platform was significantly higher than that in the model group. Both groups were lower than the control group. Conclusion: administration of melatonin in neonatal rats with bilirubin brain injury can increase the expression of bcl-2, inhibit the expression of bax, decrease the expression of NSE, and play a neuroprotective role. It can improve the learning and memory impairment caused by bilirubin related brain injury.
【學位授予單位】：桂林醫(yī)學院
【學位級別】：碩士
【學位授予年份】：2012
【分類號】：R722.17

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