本文選題：膜性腎病 + 足細(xì)胞　； 參考：《華中科技大學(xué)》2014年博士論文

【摘要】：第一部分、PHN大鼠足細(xì)胞損傷和凋亡的研究目的制備膜性腎病經(jīng)典的動(dòng)物模型被動(dòng)Heymann腎炎(PHN),觀察疾病進(jìn)程中足細(xì)胞的損傷,探討是否存在足細(xì)胞的凋亡。方法采用1月齡SPF級(jí)的SD雄性大鼠通過(guò)靜脈注射兔抗大鼠FX1A抗血清建立大鼠PHN模型并隨機(jī)分為4組:分別在模型建立后的第2、4、7、21天時(shí)處死大鼠并取材,每組8只;同時(shí)設(shè)立對(duì)照組,進(jìn)行同樣的處理。臨床生化分析儀檢測(cè)大鼠的血肌酐、尿素氮以及24小時(shí)尿蛋白總量;病理染色和透射電鏡觀察PHN模型鼠疾病進(jìn)程中的病理改變和足細(xì)胞的損傷;免疫組織化學(xué)染色檢測(cè)PHN大鼠腎小球內(nèi)C5b-9隨時(shí)間進(jìn)展的沉積;足細(xì)胞標(biāo)志蛋白WT1免疫組化染色標(biāo)記足細(xì)胞并通過(guò)Weibel-Gomez方法計(jì)數(shù)單個(gè)腎小球足細(xì)胞數(shù)量,評(píng)估足細(xì)胞出現(xiàn)明顯缺失的時(shí)間點(diǎn);活性caspase3的免疫組化染色和tunel染色評(píng)估PHN大鼠腎小球足細(xì)胞的凋亡。結(jié)果(1)造模后第2天即可觀察到C5b-9在腎小球基底膜部分階段沉積,第4天起沿基底膜呈線狀沉積,并隨疾病進(jìn)展沉積逐漸增多;PASM染色顯示隨疾病進(jìn)展腎小球基底膜逐漸增厚至21天時(shí)呈現(xiàn)明顯的局灶性階段性增厚;透射電鏡觀察顯示逐漸出現(xiàn)上皮下顆粒狀電子致密物的沉積及足突融合,至第21天可見(jiàn)典型膜性腎病改變;尿蛋白定量結(jié)果顯示,造模第3天起尿蛋白排出量即有明顯升高,至第21天時(shí)可高達(dá)50.6±6.0mg/24h; (2)造模后第21天時(shí)觀察到單位腎小球足細(xì)胞絕對(duì)數(shù)目的顯著降低(vs對(duì)照組,p0.05); (3)活性Caspase-3和TUNEL染色結(jié)果一致顯示造模后第21天腎小球內(nèi)可檢出凋亡的足細(xì)胞。結(jié)論成功制備了膜性腎病的動(dòng)物模型PHN,觀察了膜性腎病典型的病理改變進(jìn)程,足細(xì)胞損傷是其病變的核心環(huán)節(jié),在造模后第21天時(shí)觀察到足細(xì)胞的凋亡。第二部分、調(diào)控自噬對(duì)PHN大鼠足細(xì)胞損傷的影響目的 (1)觀察不同時(shí)間點(diǎn)足細(xì)胞自噬激活的改變;(2)通過(guò)自噬增強(qiáng)劑雷帕霉素和抑制劑3-甲基腺嘌呤(3-MA)調(diào)控自噬,探討調(diào)控足細(xì)胞自噬對(duì)PHN疾病進(jìn)展和足細(xì)胞損傷的影響。方法 (1)制備PHN模型鼠,并在2、4、7、21天時(shí)分別處死;(2)制備PHN模型鼠,隨機(jī)分為三組,分別給予生理鹽水、雷帕霉素溶劑、3-MA溶劑干預(yù),同時(shí)設(shè)立空白對(duì)照組和DMSO溶劑對(duì)照組,21天時(shí)處死大鼠并取材。透射電鏡觀察足細(xì)胞自噬泡數(shù)量的改變,western blot檢測(cè)自噬標(biāo)記蛋白的改變;全自動(dòng)生化分析儀測(cè)定24h尿蛋白定量、血清BUN及Cr;免疫熒光染色檢測(cè)腎小球內(nèi)C5b-9的沉積;PASM染色和透射電鏡觀察腎臟病變和足細(xì)胞損傷;Weibel-Gomez方法計(jì)數(shù)單位腎小球足細(xì)胞數(shù)量;活性caspase-3的免疫組化染色觀察凋亡的足細(xì)胞,western blot半定量分析腎小球內(nèi)細(xì)胞的凋亡。結(jié)果 (1) PHN疾病進(jìn)程中伴隨著足細(xì)胞自噬的激活,自噬增強(qiáng)劑雷帕霉素和抑制劑3-MA可以起到調(diào)控足細(xì)胞自噬的作用。(2)調(diào)控自噬不會(huì)影響PHN模型鼠的損傷因素C5b-9在腎小球的沉積。(3)雷帕霉素增強(qiáng)自噬可以改善PHN大鼠腎小球基底膜增厚的程度和范圍,減少腎小球固有細(xì)胞尤其是足細(xì)胞的凋亡,改善PHN大鼠足細(xì)胞的缺失,進(jìn)而明顯減輕PHN模型鼠蛋白尿的排出。(4) 3-MA抑制自噬明顯加重PHN大鼠腎小球基底膜增厚的程度和范圍,加重足細(xì)胞的損傷,足細(xì)胞凋亡明顯增加,足細(xì)胞缺失更加明顯,蛋白尿排除明顯增加。結(jié)論在PHN的病變過(guò)程中,自噬發(fā)揮著保護(hù)作用,適度增強(qiáng)自噬可以減少足細(xì)胞的凋亡,進(jìn)而減輕腎臟病變,緩解蛋白尿;相反,當(dāng)自噬被抑制后,足細(xì)胞損傷加重,進(jìn)而加重腎臟病變和蛋白尿程度,自噬可能是足細(xì)胞對(duì)抗補(bǔ)體介導(dǎo)的細(xì)胞損傷的機(jī)制之一。第三部分、自噬保護(hù)PHN大鼠足細(xì)胞的機(jī)制研究目的 (1)觀察PHN疾病進(jìn)程中足細(xì)胞內(nèi)質(zhì)網(wǎng)(ER)的損傷和內(nèi)質(zhì)網(wǎng)應(yīng)激(ERS)激活的變化過(guò)程,推測(cè)其和足細(xì)胞凋亡及自噬的關(guān)系;(2)觀察增強(qiáng)或者抑制自噬后ER損傷的改變及ERS信號(hào)分子的變化,探討自噬減少PHN大鼠足細(xì)胞凋亡的可能機(jī)制。方法透射電鏡觀察足細(xì)胞ER的損傷;免疫印跡檢測(cè)ERS相關(guān)蛋白的表達(dá)。結(jié)果 (1)足細(xì)胞的ER在PHN疾病進(jìn)程中損傷逐漸加重,表現(xiàn)為內(nèi)質(zhì)網(wǎng)腔擴(kuò)張、核糖體脫落等;(2) ERS相關(guān)蛋白在PHN疾病早期(第2天)表達(dá)上調(diào),早于LC3表達(dá)上調(diào)的時(shí)間;(3)增強(qiáng)足細(xì)胞的自噬水平后ER損傷明顯緩解并且ERS相關(guān)蛋白表達(dá)下調(diào),足細(xì)胞自噬被抑制后ER的損傷明顯加重同時(shí)ERS相關(guān)蛋白表達(dá)上調(diào)。結(jié)論自噬發(fā)揮減緩PHN疾病進(jìn)程并減輕足細(xì)胞損傷的作用可能是通過(guò)緩解足細(xì)胞內(nèi)質(zhì)網(wǎng)應(yīng)激的強(qiáng)度和持續(xù)的時(shí)間實(shí)現(xiàn)的,進(jìn)而調(diào)控內(nèi)質(zhì)網(wǎng)應(yīng)激的生存前信號(hào)和凋亡前信號(hào)通路,減少足細(xì)胞凋亡。調(diào)節(jié)“內(nèi)質(zhì)網(wǎng)應(yīng)激一自噬”信號(hào)途徑可能是治療膜性腎病的新途徑。
[Abstract]:The first part, the study of PHN rat foot cell injury and apoptosis to prepare the classic animal model of membranous nephropathy, passive Heymann nephritis (PHN), observe the injury of foot cells in the course of disease, and explore the existence of the apoptosis of podocyte. Methods 1 month old SPF SD male rats were used to establish rats by intravenous anti rat FX1A antiserum. The PHN model was randomly divided into 4 groups: the rats were killed and selected at the 2,4,7,21 day after the model establishment, and 8 rats in each group were selected. At the same time, the control group was set up to do the same treatment. The serum creatinine, urea nitrogen and the total amount of urine protein in the 24 hours were detected by the clinical biochemical analyzer. The pathological staining and transmission electron microscopy were used to observe the disease process of the PHN model rats. Pathological changes and injury of podoni; immunohistochemical staining was used to detect the deposition of C5b-9 in the glomeruli of PHN rats; podocyte WT1 immunohistochemical staining was used to mark the podocyte and count the number of individual glomerular podocytes by Weibel-Gomez method. Immunohistochemical staining and TUNEL staining were used to evaluate the apoptosis of glomerular podocytes in PHN rats. Results (1) the deposition of C5b-9 in the part of the glomerular basement membrane was observed on the second day after modeling, and the basement membrane was linearly deposited on the fourth day and gradually increased with the progression of the disease. PASM staining showed that the glomerular basement membrane gradually thickened with the disease progression. 21 days showed a significant focal stage thickening, and the transmission electron microscopy showed that the deposition of granular electronic dense substance and the fusion of the podocyte process gradually appeared on the twenty-first day, and the urine protein quantitative results showed that the excretion of proteinuria was significantly higher in third days and up to 50.6 + 6.0mg to twenty-first days. /24h; (2) the absolute number of glomerular podocytes was significantly reduced at twenty-first days after modeling (vs control group, P0.05), and (3) active Caspase-3 and TUNEL staining results showed that the apoptotic podonus could be detected in the glomeruli after twenty-first days of modeling. Conclusion the animal model of membranous nephropathy was successfully prepared in animal model, and the typical membranous nephropathy was observed. Histopathological process, podocyte injury is the core of the disease. The apoptosis of podropodal was observed twenty-first days after the model. The second part was to regulate the effect of autophagy on the foot cell injury in PHN rats (1) to observe the changes of autophagy at different time points, and (2) the autophagic enhancer rapamycin and the inhibitor 3- methyl adenine. Methotrexate (3-MA) regulates autophagy and regulates the effect of autophagy on the progression of PHN disease and podocyte injury. Methods (1) PHN model rats were prepared and killed at 2,4,7,21 days. (2) PHN model rats were prepared and randomly divided into three groups, which were given saline, rapamycin solvent and 3-MA solvent, and blank control group and DMSO solvent were set up at the same time. In the control group, rats were killed and selected at 21 days. The changes in the number of autophagic vesicles were observed by transmission electron microscopy. Western blot was used to detect the changes in the autophagic markers. The automatic biochemical analyzer was used to determine the quantity of 24h urine protein, the serum BUN and Cr; the immunofluorescence staining was used to detect the deposition of C5b-9 in the glomeruli; PASM staining and transmission electron microscopy were used to observe the renal lesions and the renal pathological changes. Foot cell injury; Weibel-Gomez method counts the number of unit glomerular podocytes; active caspase-3 immunohistochemical staining observation of apoptotic podocytes, Western blot semi quantitative analysis of the apoptosis of glomerular cells. Results (1) the process of PHN disease accompanied by the activation of autophagy, autophagic enhancer rapamycin and inhibitor 3-MA Play the role of regulating autophagy of podropodal. (2) Regulation of autophagy does not affect the damage factor of PHN model rats C5b-9 in the glomerular deposition. (3) the enhancement of autophagy by rapamycin can improve the extent and scope of the thickening of the glomerular basement membrane in PHN rats, reduce the apoptosis of the glomerular innate cells, especially podropodal, and improve the deletion of the podroblast in the PHN rats. And then obviously alleviated the excretion of proteinuria in the PHN model rats. (4) the inhibition of autophagy by 3-MA significantly aggravated the extent and scope of the thickening of the glomerular basement membrane in PHN rats, aggravated the injury of the Poddar cells, the apoptosis of the Poddar increased obviously, the deletion of podocytes was more obvious, and the exclusion of proteinuria increased obviously. Conclusion autophagy plays a protective role in the process of PHN disease. Appropriate enhancement of autophagy can reduce the apoptosis of the poddate, and then reduce the renal disease and alleviate the proteinuria. On the contrary, when the autophagy is suppressed, the injury of the Poda is aggravated, and then the renal disease and the degree of proteinuria are aggravated. Autophagy may be one of the mechanisms of the cell damage mediated by the podocyte. The third part, autophagy protects the PHN rat foot. The mechanism of cell study (1) observe the changes in the injury of the endoplasmic reticulum (ER) and the activation of endoplasmic reticulum stress (ERS) during the process of PHN disease, speculate on the relationship with the apoptosis of podocytes and autophagy, and (2) to observe the changes of ER damage and the change of ERS signal molecules after autophagy, and to explore the autophagy to reduce the foot cell withering in PHN rats. The possible mechanism of ER was observed by transmission electron microscopy. The expression of ERS related proteins was detected by Western blot. Results (1) the ER of podocytes increased gradually in the process of PHN disease, manifested as endoplasmic reticulum dilation, ribosome exfoliation and so on. (2) the expression of ERS related protein was up regulation in the early stage of PHN disease (second days), earlier than LC3 expression. (3) (3) after the enhancement of autophagy, the damage of the ERS related protein was obviously reduced and the expression of ERS related protein was down. The damage of ER was obviously aggravated and the expression of ERS related protein was up regulated after the autophagy was inhibited. It is possible to regulate the signal pathway of the pre subsistence signal and pre apoptotic signal pathway for endoplasmic reticulum stress and reduce the apoptosis of the Poda. The regulation of "endoplasmic reticulum stress a autophagy" signal pathway may be a new approach to the treatment of membranous nephropathy.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2014
【分類號(hào)】：R726.9

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