發(fā)布時(shí)間：2018-05-23 13:20

  本文選題：AQP2 + 七氟醚��； 參考：《吉林大學(xué)》2012年碩士論文

【摘要】：背景和目的：腎臟缺血-再灌注損傷（ischemia reperfusion,IRI）是臨床醫(yī)療中常見的病理生理過程，急性腎小管壞死（ATN）是該過程中重要和關(guān)鍵的環(huán)節(jié)。AQP2是水通道蛋白家族(AQPS)中的一種，位于腎臟集合管主細(xì)胞管腔側(cè)和靠管腔側(cè)的囊泡內(nèi)~[1,2]，是調(diào)節(jié)腎臟集合管對(duì)水通透性的主要水通道蛋白，在腎臟缺血-再灌注損傷后12-48小時(shí)表達(dá)顯著減低~[3~4]。七氟醚對(duì)心~[5~7]、腦~[8-10]、肝~[11]、肺~[12,13]等臟器和組織I/R損傷都有不同程度的保護(hù)作用已經(jīng)被證實(shí)，在學(xué)術(shù)界七氟醚預(yù)處理對(duì)腎臟缺血-再灌注是否具有保護(hù)作用仍未成定論，本實(shí)驗(yàn)詣探討大鼠腎缺血-再灌注后AQP2的表達(dá)和吸入麻醉劑七氟醚預(yù)處理對(duì)急性腎缺血再灌注損傷的保護(hù)作用。 方法：SD大鼠隨機(jī)分為假手術(shù)組（B）、對(duì)照組(I/R組)和七氟醚預(yù)處理組（Pre-S），常溫下建立大鼠急性腎缺血再灌注損傷模型,缺血再灌注后24h用生化分析儀分別檢測(cè)血清尿素氮(BUN)、肌酐(Cr)，用相應(yīng)試劑盒檢測(cè)超氧化物歧化酶(SOD)、丙二醛(MDA)；采集術(shù)前和術(shù)后24小時(shí)尿樣，，檢測(cè)尿量、尿比重；采用Real Time RT-PCR及免疫組織化學(xué)法測(cè)定腎髓質(zhì)AQP2mRNA及蛋白表達(dá)情況，觀察腎組織的病理學(xué)變化。探討七氟醚于缺血前、后處理腎臟損傷程度。 結(jié)果：與B組比較,其它兩組血清BUN、Cr，及MDA水平顯著增加(P0.05), Pre-S組BUN、Cr、MDA低于I/R組(P 0.05)。與B組比較,其它兩組SOD明顯下降，與I/R組比較, Pre-S組SOD升高。與B組比較，其它兩組尿量增加，尿比重降低，Pre-S組尿量低于I/R組(P0.05)，尿比重高于I/R組。光學(xué)顯微鏡下I/R組腎小管結(jié)構(gòu)破壞嚴(yán)重，間質(zhì)充血，水腫明顯，有大量炎細(xì)胞侵潤(rùn)，Pre-S組結(jié)構(gòu)僅見部分腎小管上皮細(xì)胞輕度腫脹,輕微變性,無明顯壞死,腎間質(zhì)水腫，充血，炎性細(xì)胞浸潤(rùn)不明顯，Pre-S組腎組織病理?yè)p傷分級(jí)明顯低于I/R組(P0.05)。腎髓質(zhì)AQP2mRNA及蛋白表達(dá)下降，Pre-S組較I/R組下降輕微(P0.05)。 結(jié)論： （1）AQP2在腎臟缺血45min,再灌注損傷24小時(shí)后表達(dá)顯著減低。 （2）七氟醚預(yù)處理對(duì)大鼠急性腎缺血再灌注損傷具有保護(hù)作用。 （3）七氟醚上調(diào)腎臟缺血-再灌注損傷后AQP2的表達(dá)。
[Abstract]:Background & objective: renal ischemia-reperfusion injury (IRI) is a common pathophysiological process in clinical medicine. Acute tubular necrosis (ATN) is an important and key link in this process. AQP2 is one of aquaporin family AQPSs. Located in the lumen side of the main cell of the renal collecting duct and the side of the lumen, it is the main aquaporin that regulates the water permeability of the renal collecting duct, and the expression of ~ (34) is significantly decreased 12-48 hours after the renal ischemia-reperfusion injury. The protective effects of sevoflurane on I / R damage in organs and tissues such as heart, brain, liver, lung and so on have been proved to be of different degrees. Whether sevoflurane preconditioning has protective effect on renal ischemia-reperfusion in academic circles has not been concluded. The purpose of this study was to investigate the expression of AQP2 and the protective effect of sevoflurane preconditioning on acute renal ischemia-reperfusion injury in rats. Methods Twenty SD rats were randomly divided into sham-operation group (control group) and sevoflurane preconditioning group (Pre-Sn). Acute renal ischemia-reperfusion injury model was established at room temperature in rats. The serum urea nitrogen bun, creatinine, superoxide dismutase (SOD), malondialdehyde (MDA) MDAA were detected by biochemical analyzer 24 hours after ischemia and reperfusion, and urine volume and specific gravity of urine were measured 24 hours before and 24 hours after reperfusion. The expression of AQP2mRNA and protein in renal medulla was determined by Real Time RT-PCR and immunohistochemistry, and the pathological changes of renal tissue were observed. To investigate the degree of renal injury after sevoflurane treatment before and after ischemia. Results: compared with group B, the serum levels of BUNC and MDA in the other two groups were significantly higher than those in group B (P 0.05), and the levels of Pre-S in group B were lower than those in group I / R (P 0.05). Compared with group B, SOD in the other two groups was significantly decreased, and SOD in Pre-S group was higher than that in group I / R. Compared with group B, the urine volume of the other two groups was increased, the urine specific gravity of Pre-S group was lower than that of I / R group (P 0.05), and the urine specific gravity was higher than that of I / R group. In the I / R group, the tubule structure was seriously damaged, interstitial hyperemia and edema were observed under optical microscope, and a large number of inflammatory cells infiltrated the pre-S group. Only some tubule epithelial cells were slightly swollen, slightly degenerated, no obvious necrosis, edema, hyperemia, and hyperemia were observed in the I / R group. The pathological grade of renal tissue in Pre-S group was significantly lower than that in I / R group (P 0.05). The expression of AQP2mRNA and protein in renal medulla decreased slightly in Pre-S group than in I / R group (P 0.05). Conclusion: The expression of AQP2 was significantly decreased after renal ischemia for 45 min and reperfusion injury for 24 hours. 2) sevoflurane preconditioning has protective effect on acute renal ischemia reperfusion injury in rats. Sevoflurane upregulated the expression of AQP2 after renal ischemia-reperfusion injury.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R363

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