本文關(guān)鍵詞： p53 急性腎損傷 PFT-α 凋亡 缺血再灌注　出處：《南京大學(xué)》2011年碩士論文　論文類型：學(xué)位論文

【摘要】：實(shí)驗(yàn)一P53在缺血再灌注導(dǎo)致急性腎損傷小鼠腎臟的表達(dá) 目的：探討缺血再灌注致急性腎損傷(AKI)小鼠腎臟不同部位p53的表達(dá)及細(xì)胞凋亡的變化。方法：采用隨機(jī)對(duì)照動(dòng)物實(shí)驗(yàn)方法,將12只小鼠隨機(jī)分為兩組：假手術(shù)組和AKI組,每組6只。采用雙側(cè)腎蒂夾閉45 min后松開動(dòng)脈夾的方法建立小鼠AKI模型,于建模后48 h采血檢測尿素氮、肌酐,取腎臟組織行HE染色觀察腎組織病理學(xué)變化,采用Western Blot法測定p53蛋白含量,免疫熒光法確定腎臟不同部位p53的表達(dá),TUNEL法檢測腎臟細(xì)胞凋亡,免疫組化方法檢測TNFR、Caspase-3及Bcl-2蛋白水平。結(jié)果：(1)AKI組小鼠血尿素氮和肌酐水平均明顯高于假手術(shù)組(P0.01)；HE染色顯示假手術(shù)組腎組織細(xì)胞形態(tài)完整,排列整齊,無明顯病理改變,AKI組則表現(xiàn)為腎小管上皮細(xì)胞刷狀緣脫落、空泡及滴狀變性,皮髓質(zhì)間有明顯淤血帶；(2)p53在假手術(shù)組小鼠腎臟無表達(dá),而AKI組小鼠缺血再灌注48h后p53蛋白則明顯增加(P0.05),并且主要在腎皮質(zhì)表達(dá)；(3)假手術(shù)組小鼠腎臟未檢測到凋亡細(xì)胞,AKI組小鼠腎臟凋亡細(xì)胞指數(shù)明顯增加(P0.01)；TNFR蛋白及Caspase-3蛋白水平升高(P0.01),Bcl-2蛋白水平下降(P0.01)。結(jié)論：急性腎損傷時(shí),腎組織p53表達(dá)增加,主要定位于皮質(zhì),并可能參與介導(dǎo)細(xì)胞凋亡 實(shí)驗(yàn)二急性腎損傷小鼠腎臟P53表達(dá)與細(xì)胞凋亡的關(guān)系 目的：探討缺血再灌注致AKI小鼠腎臟p53的表達(dá)與細(xì)胞凋亡的關(guān)系。 方法：采用隨機(jī)對(duì)照動(dòng)物實(shí)驗(yàn)方法,將18只小鼠隨機(jī)分為三組：假手術(shù)組、AKI組及PFT-α組,每組6只。采用雙側(cè)腎蒂夾閉45 min后松開動(dòng)脈夾的方法建立小鼠AKI模型,PFT-α組于建模前5 min腹腔注射p53抑制劑(PFT-α)2.2mg/kg,并于建模后48 h采血檢測尿素氮、肌酐,取腎臟組織行HE染色觀察腎組織病理學(xué)變化,采用Western Blot法測定p53蛋白含量,TUNEL法檢測腎臟細(xì)胞凋亡免疫組化方法檢測(?)TNFR、Caspase-3及Bcl-2蛋白水平。結(jié)果：(1)PFT-α組和AKI組小鼠血尿素氮、肌酐水平均明顯高于假手術(shù)組,而PFT-α組與AKI組比較血尿素氮、肌酐水平明顯降低(P0.01)；腎組織HE染色顯示AKI組腎小管上皮細(xì)胞刷狀緣脫落、空泡及滴狀變性,皮髓質(zhì)間有明顯淤血帶；PFT-α組腎小管上皮部分刷狀緣脫落消失,空泡及滴狀變性減輕,皮髓質(zhì)間無明顯淤血帶；(2)與AKI組相比,PFT-α組小鼠腎臟p53蛋白含量減少(P0.01),凋亡細(xì)胞指數(shù)也明顯減少(P0.01); TNFR蛋白及Caspase-3蛋白水平也明顯降低(P0.01), Bcl-2蛋白水平升高(P0.01)。結(jié)論：急性腎損傷時(shí),p53可能通過調(diào)控凋亡蛋白Bcl-2.、TNFR蛋白水平,促進(jìn)Caspase-3的釋放,從而介導(dǎo)細(xì)胞凋亡。
[Abstract]:Expression of p53 in Kidney of mice with Acute Renal injury induced by Ischemia and reperfusion. Objective: to investigate the expression of p53 and apoptosis in different parts of kidney of acute renal injury (AKI) mice induced by ischemia-reperfusion. Methods: twelve mice were randomly divided into two groups: sham operation group and AKI group. The AKI model of mice was established by bilateral renal pedicle occlusion for 45 min and release of artery clamp. Blood samples were collected 48 hours after modeling to detect urea nitrogen and creatinine, and kidney tissues were stained with HE to observe the pathological changes of renal tissue. Western Blot method was used to detect p53 protein content, and immunofluorescence assay was used to determine the expression of p53 in different parts of kidney. Apoptosis of renal cells was detected by Tunel method. Results the levels of blood urea nitrogen and creatinine in the control group were significantly higher than those in the sham operation group. In the AKI group, the brush edge of renal tubular epithelial cells was shedding, vacuolation and degenerative, and there was no expression of p53 in the kidney of sham-operated mice. In AKI group, p53 protein increased significantly 48 hours after ischemia and reperfusion, and was mainly expressed in renal cortex. No apoptotic cells were detected in kidney of AKI group. The apoptotic cell index of kidney in AKI group was significantly higher than that in control group. Both P0.01 TNFR protein and Caspase-3 egg were significantly increased in AKI group. The level of Bcl-2 protein decreased with the increase of white level. Conclusion: during acute renal injury, the expression of Bcl 2 protein is decreased in patients with acute renal injury. The expression of p53 in renal tissue is increased, mainly located in the cortex, and may be involved in mediating apoptosis. The relationship between the expression of p53 and apoptosis in the Kidney of mice with Acute Renal injury. Aim: to investigate the relationship between the expression of p53 and apoptosis in the kidney of AKI mice induced by ischemia reperfusion. Methods: eighteen mice were randomly divided into three groups: sham-operated group and PFT- 偽 group. Six rats in each group were treated with bilateral renal pedicle occlusion for 45 min and then loosened the artery clamp. The AKI model was established by intraperitoneal injection of p53 inhibitor PFT- 偽 2.2 mg / kg at 5 min before modeling. Blood urea nitrogen and creatinine were measured 48 h after modeling. The histopathological changes of renal tissues were observed by HE staining. The content of p53 protein was determined by Western Blot method and the apoptosis of renal cells was detected by Tunel method. Results the levels of blood urea nitrogen and creatinine in the two groups were significantly higher than those in the sham operation group, and the blood urea nitrogen levels in the PFT- 偽 group and the AKI group were significantly higher than those in the AKI group, the levels of Caspase-3 and Bcl-2 protein in the TNFR- 偽 group were significantly higher than those in the sham operation group. The renal tissue HE staining showed that the brush edge, vacuole and degeneration of renal tubule epithelium in AKI group were obviously decreased, and that in PFT- 偽 group, the tubule epithelium brushed edge disappeared, vacuolation and droplet degeneration were alleviated in PFT- 偽 group. Compared with AKI group, the content of p53 protein in kidney of PFT- 偽 group decreased significantly, the apoptotic cell index also decreased significantly, the levels of TNFR protein and Caspase-3 protein decreased significantly, and the level of Bcl-2 protein increased P0.01a. Conclusion: P0.01protein level of PFT- 偽 group is higher than that of PFT- 偽 group, and the apoptotic cell index of P0.01a group is significantly lower than that of PFT- 偽 group, and the level of TNFR protein and Caspase-3 protein is also significantly lower than that of AKI group. During renal injury, p53 may regulate the level of apoptotic protein Bcl-2. Promote the release of Caspase-3, thus mediating cell apoptosis.
【學(xué)位授予單位】：南京大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2011
【分類號(hào)】：R363

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