本文選題：急性腎缺血再灌注損傷 + 內(nèi)質(zhì)網(wǎng)應激　； 參考：《福建醫(yī)科大學》2014年碩士論文

【摘要】：目的： 腎臟急性缺血再灌注損傷是臨床非常重要的一個問題。目前對于其發(fā)病機理還缺乏認識，因此也還沒有找到有針對性的有效治療措施。本課題通過尋找到對腎臟急性缺血再灌注損傷存在抗性的小鼠種系，通過與容易發(fā)生損傷的小鼠腎臟進行比較來探索導致腎臟急性缺血再灌注損傷的關鍵的致病分子，目的是在了解腎臟急性缺血再灌注損傷分子發(fā)病機制的基礎上研發(fā)靶向治療藥物。 方法： 將FVB、ICR兩種小鼠（雄性♂、8-10W）各隨機分為正常組和模型組(n=6)，兩種小鼠模型組應用先切除右腎再夾閉左腎腎蒂45min的方法來建立急性腎缺血再灌注損傷模型，再灌注24小時后收集模型組小鼠的心臟血、腎臟，應用脲酶法檢測各小鼠血漿BUN濃度，采用PAS染色觀察小鼠腎組織病理損傷的程度，PCR、 Western-blot檢測腎組織chop mRNA、CHOP蛋白的表達，正常組檢測同樣的指標。 結(jié)果： （1）腎組織PAS染色可見：FVB、ICR小鼠模型組腎小管上皮細胞損傷明顯重于正常組，有明顯的統(tǒng)計學意義（P0.01），ICR鼠模型組腎小管上皮細胞損傷又明顯重于FVB鼠模型組，有明顯的統(tǒng)計學意義（P0.01）；（2）血漿BUN濃度：FVB、ICR小鼠模型組高于正常組，有明顯的統(tǒng)計學意義（P0.01），ICR鼠模型組高于FVB鼠模型組，有明顯的統(tǒng)計學意義（P0.01）；（3）PCR：各組之間chop mRNA表達無明顯差異（P0.05）；（4）Western-blot：FVB、ICR小鼠模型組CHOP蛋白的表達量高于正常組，有明顯的統(tǒng)計學意義（P0.01），ICR小鼠模型組CHOP蛋白的表達量高于FVB鼠模型組（P0.05）。 結(jié)論： 在急性腎缺血再灌注損傷模型中ICR小鼠腎小管上皮細胞損傷程度明顯重于FVB小鼠，內(nèi)質(zhì)網(wǎng)應激相關蛋白CHOP表達也明顯上調(diào)，提示CHOP在急性腎缺血再灌注損傷中發(fā)揮了重要的作用，，F(xiàn)VB小鼠對急性腎缺血再灌注損傷存在抗性，機制可能與CHOP蛋白的表達有關。
[Abstract]:Objective:Acute renal ischemia reperfusion injury is a very important clinical problem.At present, there is a lack of understanding of its pathogenesis, so no targeted and effective treatment has been found.In this study, we find the strain of mice resistant to acute renal ischemia-reperfusion injury, and explore the key pathogenic molecules that lead to acute renal ischemia-reperfusion injury by comparing them with those prone to renal injury.The aim of this study was to investigate the molecular pathogenesis of acute renal ischemia reperfusion injury.Methods:Two kinds of mice (male) were randomly divided into two groups: normal group and model group. The models of acute renal ischemia-reperfusion injury were established by removing the right kidney and then clipping the left kidney pedicle 45min.After 24 hours of reperfusion, the heart blood and kidney of the model group were collected. The plasma BUN concentration of each mouse was detected by urease method. The degree of renal pathological injury was observed by PAS staining. The expression of chop mRNA-chop protein in renal tissue was detected by Western-blot.The same index was detected in the normal group.Results:(1) PAS staining of renal tissue showed that the injury of renal tubular epithelial cells in the PAS group was significantly more serious than that in the normal group, and the injury of renal tubular epithelial cells in the model group was significantly more serious than that in the FVB model group.There was significant statistical significance (P 0.01) the plasma BUN concentration in the model group was higher than that in the normal group, and it was significantly higher in the model group than that in the FVB group.There was no significant difference in the expression of chop mRNA between the two groups. The expression of CHOP protein in the Western-blot1: FVB-ICR model group was higher than that in the normal group, and the expression of CHOP protein in the P0.01 / FVB model group was significantly higher than that in the FVB model group (P0.05).Conclusion:In acute renal ischemia-reperfusion injury model, the injury degree of renal tubular epithelial cells in ICR mice was significantly greater than that in FVB mice, and the expression of endoplasmic reticulum stress-related protein (CHOP) was up-regulated.The results suggest that CHOP plays an important role in acute renal ischemia-reperfusion injury. FVBmice are resistant to acute renal ischemia-reperfusion injury, and the mechanism may be related to the expression of CHOP protein.
【學位授予單位】：福建醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R692


本文編號：1734215