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  本文選題：缺血再灌注損傷 + 缺血半暗帶��； 參考：《廣西醫(yī)科大學》2013年碩士論文

【摘要】：目的：觀察大鼠急性腦缺血再灌注損傷后,缺血半暗帶腦組織Na+-K+-ATP酶活性的動態(tài)變化,以及腦蛋白水解物和銀杏葉提取物對該酶活性的影響,探討腦蛋白水解物及銀杏葉提取物聯(lián)合應用對大鼠缺血半暗帶神經(jīng)元的保護作用及機制。 方法：將600只雄性Wistar大鼠通過數(shù)字表法隨機分為對照組、蛋白組、銀杏葉組、聯(lián)合組,共4組,每組大鼠根據(jù)缺血后再灌注時間的不同又分為缺血2h再灌注6h、24h、48h、72h、7d五個亞組,其中每個亞組大鼠為30只。用10%水合氯醛350mg/kg腹腔注射麻醉大鼠,參照Longa等介紹的栓線法制備大鼠缺血2h再灌注模型,采用Zea Longa評分法判定動物模型與否成功。除對照組外,其余三組均于大鼠造模后5h至斷頭取腦時每日用藥物進行干預一次。腦蛋白組:5ml/kg腦蛋白水解物注射液,銀杏葉組：100mg/kg銀杏葉提取物注射液,聯(lián)合組：5ml/kg腦蛋白水解物注射液及100mg/kg銀杏葉提取物注射液。各亞組大鼠分別于缺血再灌注6h,24h,48h,72h及7d斷頭取腦,觀察缺血半暗帶腦組織Na+-K+-ATP酶活性、腦組織水腫程度、腦梗死范圍及神經(jīng)癥狀評分的變化。 結(jié)果： 1.6h時對照組大鼠腦缺血半暗帶神經(jīng)元Na+-K+-ATP酶的活性為(4.810±0.426) U/mg,隨著缺血再灌注時間的延長,Na+-K+-ATP酶的活性逐漸降低,于48h達最低值(3.537±0.415) U/mg,72h稍有回升(3.671+0.501) U/mg,7d趨于穩(wěn)定(5.022±0.623) U/mg。值得注意的規(guī)律是,隨著缺血再灌注時間的推移,腦組織缺血半暗帶神經(jīng)元Na+-K+-ATP酶活性呈下降趨勢,與此同時,腦組織含水量及梗死面積卻在逐漸增加。 2.6h時,對照組、蛋白組、銀杏葉組及聯(lián)合組四組之間Na+-K+-ATP酶活性差異無統(tǒng)計學意義(P=0.864),隨著缺血再灌注時間的延長,對照組Na+-K+-ATP酶的活性逐漸降低,而蛋白組、銀杏葉組及聯(lián)合組Na+-K+-ATP酶活性較對照組明顯升高,差異具有統(tǒng)計學意義(24h、48h及72h亞組,P值均為0.000),蛋白組與銀杏葉組之間差異無統(tǒng)計學意義(P0.05)。與單一用藥組(蛋白組或銀杏葉組)比較,聯(lián)合組能明顯提高大鼠缺血半暗帶神經(jīng)元Na+-K+-ATP酶活性(48h、72h亞組,P值均為0.000),與此同時,還能顯著降低腦組織含水量(24h、48h、72h亞組,P值均為0.000),減小腦梗死面積(24h、48h、72h、7d亞組,P值均為0.000),減少神經(jīng)癥狀評分(48h、72h、7d亞組,P值均為0.000)。 結(jié)論： 1.急性腦缺血再灌注損傷后缺血半暗帶腦組織Na+-K+-ATP酶活性呈動態(tài)變化； 2.Na+-K+-ATP酶活性變化與腦組織水腫程度、腦梗死面積大小密切相關,在缺血半暗帶腦組織缺血再灌注損傷過程中發(fā)揮著至關重要的作用。 3.聯(lián)合用藥具有協(xié)同作用,較單一用藥能更有效地抑制缺血級聯(lián)反應,從而最大限度地挽救缺血半暗帶神經(jīng)元的功能。
[Abstract]:Aim: to observe the dynamic changes of Na K ATPase activity in the brain of ischemic penumbra after acute cerebral ischemia-reperfusion injury in rats, and the effects of brain protein hydrolysate and ginkgo biloba extract on the activity of Na K ATPase. To investigate the protective effect and mechanism of brain protein hydrolysate and ginkgo biloba extract on ischemic penumbra neurons in rats. Methods: 600 male Wistar rats were randomly divided into four groups by digital table: control group, protein group, ginkgo biloba leaf group, combined group. According to the time of reperfusion after ischemia, each group was divided into five subgroups: 2 h ischemia, 24 h reperfusion and 48 h reperfusion for 72 h and 7 d. There were 30 rats in each subgroup. 10% chloral hydrate 350mg/kg was injected intraperitoneally into anesthetized rats. The model of ischemia 2 h reperfusion was made by referring to the method of suture introduced by Longa et al. The Zea Longa scoring method was used to determine whether the model was successful or not. In addition to the control group, the other three groups were treated with drugs once a day, 5 hours after the rat model was made and the brain was removed from the head. Brain protein group: 5 ml / kg brain protein hydrolysate injection, ginkgo leaf group 100 mg / kg Ginkgo biloba extract injection, combined group 5 ml / kg brain protein hydrolysate injection and 100mg/kg ginkgo leaf extract injection. The rats in each subgroup were decapitated for 72 h and 7 d respectively at 6 h, 24 h and 48 h after reperfusion. The changes of Na K ATPase activity, brain edema degree, infarct area and neurological symptom score were observed in the ischemic penumbra. Results: At 1.6 h, the activity of Na -K ATPase was 4.810 鹵0.426) U / mg in the neurons of cerebral ischemic penumbra in the control group. With the prolongation of ischemia reperfusion time, the activity of Na -K ATPase decreased gradually, and increased slightly at 48 h to the lowest value of 3.537 鹵0.415) U / mg ~ (-1) (3.671 ~ 0.501) U / (mg ~ (-1). The activity of Na ~ (-K) -ATPase increased to 5.022 鹵0.623) / 渭 mg / g at 48 h. It is worth noting that the activity of Na-K-ATPase in the neurons of the ischemic penumbra decreased with the time of ischemia and reperfusion, but the water content and the infarct area of the brain tissue increased gradually at the same time. At 2.6 h, there was no significant difference in Na K ATPase activity between control group, protein group, ginkgo biloba leaf group and combination group. The Na K ATPase activity of control group decreased gradually with the prolongation of ischemia reperfusion time, while the activity of Na K ATPase decreased in protein group. The activity of Na -K ATPase in the ginkgo leaf group and the combined group was significantly higher than that in the control group, and the difference was statistically significant (P = 0.000) between the 24 h and 72 h subgroups, but there was no significant difference between the protein group and the ginkgo leaf group (P 0.05). Compared with the single drug group (protein group or ginkgo biloba group), the combined group could significantly increase the activity of Na-K-ATPase in ischemic penumbra neurons. It also significantly decreased the water content of brain tissue (P = 0.000), decreased the area of cerebral infarction (P = 0.000), reduced the area of cerebral infarction (24 h / 48 h, 72 h / 7 d), reduced the neurological symptom score (P = 0.000) and reduced the neurological symptom score (P = 0.000) at 48h and 7h / 7d respectively in the subgroup of 24 h, 48 h, 72 h and 72 h, respectively. Conclusion: 1. After acute cerebral ischemia-reperfusion injury, the activity of Na -K ATPase in the brain tissue of ischemic penumbra showed dynamic changes. The change of 2.Na-K-ATPase activity is closely related to the degree of cerebral edema and the size of cerebral infarction. It plays an important role in the process of cerebral ischemia-reperfusion injury in ischemic penumbra. 3. The synergistic effect of combined medication can inhibit ischemic cascade reaction more effectively than that of single medication, thus saving the function of ischemic penumbra neurons to the maximum extent.
【學位授予單位】：廣西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2013
【分類號】：R743.3

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本文編號：1864134