【摘要】：目的:觀察大鼠局灶性腦缺血再灌注損傷及p-STAT3的表達(dá)情況以及實(shí)施亞低溫和異氟醚處理后的變化,探討亞低溫和異氟醚聯(lián)合治療的腦保護(hù)作用及其可能的作用機(jī)制。方法:健康雄性成年SD大鼠(Sprague-Dawley rats,SDrats)50只,體重250-300g,隨機(jī)分為5組(n=10),假手術(shù)組(Sham組)僅切開皮膚,不留置線栓;模型組(ischemia-reperfusion,I/R組)線栓法造大腦中動脈閉塞(middle cerebral artery occlusion,MCAO)模型;亞低溫組(mild hypothermia,MH組)、異氟醚后處理組(isoflurane,Iso組)分別術(shù)中持續(xù)頭部亞低溫至再灌注結(jié)束、缺血再灌注后異氟醚治療1小時。亞低溫異氟醚聯(lián)合治療組(MH+Iso組)聯(lián)合兩種治療方法。于再灌注24 h后進(jìn)行神經(jīng)功能缺陷評分(neurological deficit scores,NFC),各組取5只大鼠處死,取腦組織,2,3,5-三苯基氯化四氮唑(2,3,5-Triphenyltetrazolium chloride,TTC)染色法測定腦梗死體積;另外每組處死5只大鼠,取腦組織缺血皮層,免疫印跡(Western blotting,WB)檢測細(xì)胞蛋白表達(dá)情況,并測定p-STAT3和t-STAT3的蛋白表達(dá)水平。結(jié)果:1)與I/R組比較,MH組、Iso組、MH+Iso組神經(jīng)功能缺損評分明顯降低(P0.01),腦梗死體積顯著縮小(P0.01),p-STAT3/t-STAT3明顯減少(P0.01)。2)與MH組、Iso組相比,MH+Iso組神經(jīng)功能缺損評分降低(P0.05),腦梗死體積縮小(P0.05),p-STAT3/t-STAT3明顯減少(P0.05)結(jié)論:亞低溫聯(lián)合異氟醚后處理能顯著減少大鼠腦缺血再灌注損傷程度,效果優(yōu)于單獨(dú)亞低溫或異氟醚后處理治療,其機(jī)制可能是亞低溫聯(lián)合異氟醚后處理抑制星型膠質(zhì)細(xì)胞和小膠質(zhì)細(xì)胞酪氨酸激酶2(Janus kinase,JAK2)/轉(zhuǎn)錄因子3(signal transducer and activator of transcription3,STAT3)信號轉(zhuǎn)導(dǎo)通路的表達(dá),隨后抑制星型膠質(zhì)細(xì)胞或小膠質(zhì)細(xì)胞激活和增殖,起到腦缺血再灌注保護(hù)作用。
[Abstract]:Aim: to observe the expression of p-STAT3 and the changes of focal cerebral ischemia-reperfusion injury in rats after mild hypothermia and isoflurane treatment, and to explore the protective effect of mild hypothermia and isoflurane on brain and its possible mechanism. Methods: 50 healthy male adult SD rats (Sprague-Dawley rats,SDrats), weighing 250-300g, were randomly divided into 5 groups: sham operation group (Sham group), sham-operated group (Sham group), model group (ischemia-reperfusion,I/R group), middle cerebral artery occlusion (middle cerebral artery occlusion,MCAO) model. Mild hypothermia group (mild hypothermia,MH group) and isoflurane post-treatment group (isoflurane,Iso group) continued mild hypothermia until the end of reperfusion during operation. Isoflurane was treated with isoflurane for 1 hour after ischemia-reperfusion. Mild hypothermia isoflurane combined treatment group (MH Iso group) combined with two treatment methods. After 24 hours of reperfusion, the neurological deficit score (neurological deficit scores,NFC) was used. Five rats in each group were killed, and the cerebral infarct volume was determined by the method of 2-titration 3-triphenyltetrazolium chloride,TTC staining, and 5 rats were killed in each group, and the ischemic cortex of the brain tissue was taken. Western blot (Western blotting,WB) was used to detect the expression of p-STAT3 and t-STAT3. Results compared with the I / R group, the neurological impairment score and the infarct volume of the MH / Iso Iso group were significantly decreased (P0.01), and the volume of cerebral infarction was significantly reduced (P0.01). Compared with the MH group (P0.01), the neurological function defect score of the MH-Iso group decreased (P0.05), the cerebral infarction volume decreased (P0.01), and the cerebral infarct volume shrank significantly (P0.01) in comparison with that in the MH group (P0.01). Conclusion: mild hypothermia combined with isoflurane can significantly reduce the degree of cerebral ischemia-reperfusion injury in rats. The effect is better than that of mild hypothermia or isoflurane treatment alone. The mechanism may be that mild hypothermia combined with isoflurane post treatment inhibits the expression of tyrosine kinase 2 (Janus kinase,JAK2) / transcription factor 3 (signal transducer and activator of transcription3,STAT3 signal transduction pathway in astrocytes and microglia. Subsequently, it inhibited the activation and proliferation of astrocytes or microglia, and played a protective role in cerebral ischemia reperfusion.
【學(xué)位授予單位】：皖南醫(yī)學(xué)院
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【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：2237749