本文選題：干細胞因子 + 急性腎損傷　； 參考：《青島大學》2014年碩士論文

【摘要】：背景：細胞因子在減輕腎臟缺血再灌注損傷中的作用逐漸受到重視,干細胞因子具有造血系統(tǒng)以外的器官保護作用。 目的：探討大鼠急性腎損傷模型中干細胞因子(stem cell factor SCF)及其受體c-Kit表達的變化和促紅細胞生成素預(yù)處理對其表達的影響。 方法：成年雄性Wistar大鼠34只,采用夾閉雙側(cè)腎蒂建立缺血再灌注模型,缺血45分鐘后再灌注24小時,隨機分為假手術(shù)組(n=10)、缺血再灌注組(17=12)和促紅細胞生成素組(n=12),促紅細胞生成素組于建立模型前2小時一次性尾靜脈注射重組人促紅細胞生成素5000U/kg。采用免疫組化及圖像分析技術(shù)檢測各組腎組織中SCF及其受體c-Kit的表達變化,自動生化儀測定血清肌酐和尿素氮水平,常規(guī)蘇木精-伊紅染色觀察腎組織病理學改變并計算腎小管損傷積分。 結(jié)果：(1)SCF及c-Kit在腎組織中的表達僅限于腎小管區(qū)域。與假手術(shù)組比較,SCF和c-Kit在缺血再灌注組和促紅細胞生成素組的表達均明顯增高(P0.05,P0.01),促紅細胞生成素組SCF表達高于缺血再灌注組(P0.05),但缺血再灌注組和促紅細胞生成素組c-Kit表達差異無顯著性意義(P0.05)。(2)促紅細胞生成素組血清肌酐與尿素氮水平明顯低于缺血再灌注組(P0.05),但高于假手術(shù)組(P0.05)。(3)與假手術(shù)組比較,缺血再灌注組及促紅細胞生成素組腎組織均出現(xiàn)不同程度的損傷,促紅細胞生成素組腎組織損傷程度較缺血再灌注組明顯減輕。 結(jié)論：缺血再灌注導(dǎo)致急性腎損傷發(fā)生時SCF及c-Kit表達升高,而促紅細胞生成素對急性腎損傷的保護作用可能與上調(diào)SCF表達有關(guān)。
[Abstract]:Background: the role of cytokines in alleviating renal ischemia-reperfusion injury has been paid more attention. Stem cell factor plays an organ protective role outside the hematopoietic system.
Objective: To investigate the changes in the expression of stem cell factor SCF and its receptor c-Kit in the rat model of acute renal injury and the effect of erythropoietin preconditioning on its expression.
Methods: 34 adult male Wistar rats were established by clamping bilateral renal pedicle for ischemia reperfusion model, and reperfusion for 24 hours after 45 minutes of ischemia. They were randomly divided into sham operation group (n=10), ischemia reperfusion group (17=12) and erythropoietin group (n=12), erythropoietin group was injected into a recombinant human intravenous infusion group at one time before the establishment of the model. Erythropoietin 5000U/kg. was used to detect the expression of SCF and its receptor c-Kit in renal tissues by immunohistochemistry and image analysis. The level of serum creatinine and urea nitrogen was measured by automatic biochemical analyzer. The pathological changes of renal tissue were observed by routine hematoxylin eosin staining and the integral of renal tubule injury was calculated.
Results: (1) the expression of SCF and c-Kit in renal tissue was limited to the renal tubule region. Compared with the sham group, the expression of SCF and c-Kit in the ischemia-reperfusion group and the erythropoietin group increased significantly (P0.05, P0.01). The expression of SCF in the erythropoietin group was higher than that of the ischemia reperfusion group (P0.05), but the ischemia reperfusion group and the erythropoiesis were produced. There was no significant difference in the expression of c-Kit in the vegetarian group (P0.05). (2) the serum creatinine and urea nitrogen level in the erythropoietin group was significantly lower than that of the ischemia reperfusion group (P0.05), but higher than the sham operation group (P0.05). (3) the renal tissue of the ischemia reperfusion group and the erythropoietin group had varying degrees of damage and erythropoietin growth compared with the sham operation group. The injury degree of kidney tissue in the treated group was significantly lower than that in the ischemia-reperfusion group.
Conclusion: the expression of SCF and c-Kit in acute renal injury is increased by ischemia-reperfusion, and the protective effect of erythropoietin on acute renal injury may be related to the up-regulation of SCF expression.
【學位授予單位】：青島大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R692.5

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