發(fā)布時(shí)間：2018-08-27 19:58

【摘要】：缺血再灌注損傷是實(shí)體器官移植不可避免的一個(gè)階段,在腎移植中,因腎臟缺血再灌注損傷的存在,可顯著增加腎移植術(shù)后急性排斥反應(yīng)發(fā)生率,同樣腎小管上皮細(xì)胞的修復(fù)需要相對(duì)較長(zhǎng)一段時(shí)間,從而導(dǎo)致腎移植術(shù)后移植腎功能延遲恢復(fù),從長(zhǎng)遠(yuǎn)考慮可能會(huì)影響移植腎和受者的長(zhǎng)期存活。腎小管細(xì)胞培養(yǎng)模型、動(dòng)物實(shí)驗(yàn)和臨床研究均提示腎臟缺血再灌注損傷介導(dǎo)的腎小管上皮細(xì)胞死亡有壞死和凋亡兩種形式。早期即出現(xiàn)大量腎小管上皮細(xì)胞凋亡和壞死,腎小管上皮細(xì)胞受累后主要發(fā)生去分化,細(xì)胞骨架的完整性和極性受到損害,最終導(dǎo)致腎組織結(jié)構(gòu)破壞,從而影響腎功能。晚期在各種修復(fù)機(jī)制的作用下發(fā)生去分化的腎小管上皮細(xì)胞增殖、移行,并進(jìn)行再分化,腎小管上皮細(xì)胞增殖的逐步啟動(dòng)后,經(jīng)歷一段時(shí)間后受損的部分腎功能逐漸恢復(fù)。作為實(shí)體器官移植與缺血再灌注損傷并存的現(xiàn)狀,我們應(yīng)采取積極有效手段和方法,最大程度上抑制腎小管上皮細(xì)胞的凋亡,減輕腎臟缺血再灌注損傷帶來的不利影響,保護(hù)腎功能,對(duì)于減少腎移植術(shù)后移植腎功能延遲恢復(fù)以及急性排斥反應(yīng)發(fā)生率,最終達(dá)到延長(zhǎng)移植腎和受者的存活時(shí)間的目的,具有深遠(yuǎn)的臨床意義。 西羅莫司(SRL)是哺乳類SRL靶分子(mammalian target of rapamycin, mTOR)抑制劑,動(dòng)物實(shí)驗(yàn)和多年的臨床應(yīng)用結(jié)果均顯示,以SRL為主而不含CNI的免疫抑制方案或?qū)NI類免疫抑制劑轉(zhuǎn)換為以西羅莫司為主的免疫抑制方案后與以CNI為基礎(chǔ)的免疫抑制方案相比,能顯著降低因CNI類腎毒性造成的腎移植術(shù)后血肌酐呈爬行性上升的趨勢(shì),腎功能明顯好轉(zhuǎn)。因西羅莫司幾乎無腎臟毒性,肝毒性較低,且與CNI類為基礎(chǔ)的免疫抑制方案相比,患者的1年移植物存活率、急性排斥反應(yīng)發(fā)生率均無明顯差異,腎功能卻明顯優(yōu)于CNI組。對(duì)腎移植術(shù)后血肌酐呈階梯性、爬行性慢性上升的患者,并經(jīng)病理確診的因CNI類腎毒性和慢性移植腎病的患者,適時(shí)的進(jìn)行SRL轉(zhuǎn)換治療可明顯改善移植腎功能,延長(zhǎng)移植腎和受者的存活時(shí)間。 目前,關(guān)于SRL對(duì)缺血再灌注損傷的作用仍存在爭(zhēng)議。研究發(fā)現(xiàn)SRL可能通過以下機(jī)制明顯減輕大鼠腎臟缺血再灌注損傷和改善腎功能：(1)通過非直接通路激活T細(xì)胞凋亡程序,阻止了樹突狀細(xì)胞(DC)的抗原呈遞,并進(jìn)一步抑制其成熟；(2)減少細(xì)胞因子的分泌,阻止DC在腎組織遷移聚集；周四桂等用SRL處理經(jīng)缺氧復(fù)氧的血管內(nèi)皮細(xì)胞,通過抑制ROS、JNK、NF-κB的信號(hào)傳導(dǎo)途徑,抑制血管內(nèi)皮細(xì)胞與中性粒細(xì)胞的粘附。Yang B等發(fā)現(xiàn)使用SRL干預(yù)腎臟缺血再灌注損傷,主要是激活了24KDCaspase-3,減少凋亡的發(fā)生,同時(shí)減少遠(yuǎn)曲小管中Fas的表達(dá),通過減輕Fas信號(hào)途徑引起的免疫損傷,起到保護(hù)缺血腎臟再灌注損傷的作用。Bohmova R等在轉(zhuǎn)基因高血壓大鼠腎缺血再灌注損傷中觀察發(fā)現(xiàn),小劑量的SRL能夠減輕由于腎素產(chǎn)生過多引起的腎臟再灌注損傷。但是也有一些學(xué)者持相反的觀點(diǎn),在體外,SRL在1ng/ml時(shí)抑制鼠的近曲小管細(xì)胞的增生,同時(shí)通過抑制腎小管細(xì)胞中70kDaS6蛋白激酶來發(fā)揮促進(jìn)凋亡作用。在體內(nèi)SRL通過抑制腎小管細(xì)胞再生和增加腎小管細(xì)胞的凋亡,抑制腎缺血再灌注后腎小管的再生,影響損傷的修復(fù),從而延緩腎功能的恢復(fù)。Lui SL等報(bào)道SRL在1天、3天時(shí)降低增殖細(xì)胞核抗原(PCNA)的表達(dá),但是第7天時(shí)與對(duì)照組沒有差別,表明SRL會(huì)加重腎臟的損害主要是通過抑制腎小管細(xì)胞的再生而延緩了腎功能的恢復(fù),但并不是一直抑制腎小管細(xì)胞的再生。 在缺血再灌注損傷中,不同劑量的SRL對(duì)不同時(shí)期大鼠腎缺血再灌注損傷及腎小管上皮細(xì)胞凋亡后增殖、修復(fù)作用尚不明確。我們推測(cè),在缺血再灌注損傷早期,SRL的抗凋亡作用可能會(huì)抑制腎小管上皮細(xì)胞的壞死,起到對(duì)損傷腎臟組織的保護(hù)作用,但在后期隨著腎小管上皮細(xì)胞修復(fù)程序的逐步啟動(dòng),其抗增殖作用可能會(huì)抑制腎小管上皮細(xì)胞的細(xì)胞增殖、移行、再分化以及骨架的重建,進(jìn)而影響腎功能恢復(fù)并存在劑量的依賴性和可逆性。我們研究發(fā)現(xiàn)給于大鼠SRL3mg/(kg.d),其谷濃度為腎移植術(shù)后早期治療濃度,以此劑量為標(biāo)準(zhǔn)我們建立大鼠腎缺血再灌注損傷模型,通過檢測(cè)腎臟損傷敏感標(biāo)志物NGAL、IL-18;凋亡基因Fas、Bcl-2和PCNA蛋白表達(dá),腎小管上皮細(xì)胞修復(fù)因子HGF和BMP-7mRNA表達(dá)等方面,研究其對(duì)腎缺血再灌注損傷及腎小管上皮細(xì)胞修復(fù)的綜合影響。 第一部分西羅莫司對(duì)大鼠腎臟缺血再灌注損傷早期的保護(hù) 摘要 目的：探討西羅莫司(SRL)對(duì)不同時(shí)期大鼠腎缺血再灌注損傷的影響。 方法： 1.選用雄性SD(Sprague-Dawley)大鼠共90只,隨機(jī)均勻分為五組：sham、I/RI/R+SRL1mg/(kg.d)、I/R+SRL3mg/(kg.d)、 I/R+SRL5mg/(kg.d)。 2.建立大鼠缺血再灌注損傷模型。 3.藥物各組術(shù)前3天及術(shù)后每日給予對(duì)應(yīng)劑量SRLlmg.3mg.5mg與10ml生理鹽水灌胃至各個(gè)觀察日。 4.sham、I/R給予等量生理鹽水灌胃至各個(gè)觀察日。 5.術(shù)后1、3、7天每組各處死6只大鼠取全血及腎組織,檢測(cè)血清肌酐、p2-MG； 6. ELISA法測(cè)定中性粒細(xì)胞明膠酶相關(guān)脂質(zhì)運(yùn)載蛋白(NGAL)、IL-18； 7.HE染色評(píng)價(jià)組織病理學(xué)改變； 8.免疫組化SABC法檢測(cè)腎組織Fas、Bcl-2蛋白的表達(dá)； 9. Western-blot技術(shù)檢測(cè)Fas、Bcl-2蛋白表達(dá)強(qiáng)度； 10.脫氧核糖核苷酸末端轉(zhuǎn)移酶介導(dǎo)的缺口末端標(biāo)記(TUNEL)法檢測(cè)腎組織細(xì)胞凋亡率。 結(jié)果： 1.術(shù)后1、3天血Cr、p2-MG、IL-18、Fas和Bcl-2水平、病理學(xué)評(píng)分、Fas和Bcl-2蛋白陽性表達(dá)率、凋亡指數(shù)均升高,除Bcl-2水平外shamI/R+SRL5mg/(kg.d)I/R+SRL3mg/(kg.d)I/R+SRL1mg/(kg.d)I/R(P0.05)。 2.Bc1-2水平：][/R+SRL5mg/(kg.d)I/R+SRL3mg/(kg.d)I/R+SRL1mg/(kg.d)I/Rsham(P0.05)。 3.術(shù)后7天Fas、Bcl-2水平：I/R+SRL5mg/(kg.d)與sham和I/R+SRLlmg/(kg.d)比較有差異(P0.05)； 4. NGAL水平術(shù)后1天高于sham(P0.05)。凋亡指數(shù)I/R+SRL5mg/(kg.d)與余四組比較有差異(P0.05)。 結(jié)論： 1.成功建立大鼠腎臟缺血再灌注損傷模型。 2.西羅莫司在缺血再灌注損傷早期通過其顯著抑制腎小管上皮細(xì)胞細(xì)胞凋亡的作用,起到保護(hù)腎功能的作用。 3.西羅莫司在缺血再灌注損傷早期對(duì)腎功能保護(hù)具有劑量依賴性。 第二部分西羅莫司對(duì)大鼠腎小管上皮細(xì)胞修復(fù)的影響 摘要 目的：探討西羅莫司(SRL)對(duì)不同時(shí)期大鼠腎小管上皮細(xì)胞修復(fù)的影響。 方法： 1.選用雄性SD(Sprague-Dawley)大鼠共90只,隨機(jī)均勻分為五組：sham、I/R、I/R+SRLlmg/(kg.d)、I/R+SRL3mg/(kg.d)、 I/R+SRL5mg/(kg.d)。　 2.建立大鼠缺血再灌注損傷模型。 3.藥物各組術(shù)前3天及術(shù)后每日給予對(duì)應(yīng)劑量SRLlmg、3mg、5mg與10ml生理鹽水灌胃至各個(gè)觀察日。； 4.sham、I/R給予等量生理鹽水灌胃至各個(gè)觀察日。 5.術(shù)后1、3、7天每組各處死6只大鼠取全血及腎組織,檢測(cè)血清肌酐； 6. ELISA法測(cè)定p2-MG、肝細(xì)胞生長(zhǎng)因子(HGF)水平； 7.HE染色評(píng)價(jià)組織病理學(xué)改變； 8.免疫組化SABC法檢測(cè)腎組織增殖細(xì)胞核抗原(PCNA)蛋白的表達(dá)； 9. RT-PCR技術(shù)檢測(cè)修復(fù)因子HGF的mRNA、骨形態(tài)發(fā)生蛋白-7(BMP-7) mRNA表達(dá)。 結(jié)果： 1.術(shù)后1、3天血Cr、β2-MG、病理學(xué)評(píng)分均升高：shamI/R+SRL5mg/(kg.d)I/R+SRL3mg/(kg.d)I/R+SRL1mg/(kg.d)I/R(P0.05)； 2.術(shù)后1、3天血HGF值、HGFmRNA、BMP-7mRNA水平和1、3、7天PCNA水平：shamI/R+SRL5mg/(kg.d)I/R+SRL3mg/(kg.d)I/R+SRLlmg/(kg.d)I/R(P0.05); 3.Sham術(shù)后各時(shí)期均未見增殖細(xì)胞,余四組均有大量細(xì)胞增殖。 結(jié)論： 1.成功建立大鼠缺血再灌注損傷模型。 2.西羅莫司在缺血再灌注損傷中其抗增殖作用阻礙了腎小管上皮細(xì)胞的移行、骨架重建等修復(fù)過程。 3.西羅莫司在缺血再灌注損傷中其抗增殖作用具有劑量依賴性。
[Abstract]:Ischemia-reperfusion injury is an unavoidable stage in solid organ transplantation. In renal transplantation, the presence of ischemia-reperfusion injury can significantly increase the incidence of acute rejection after kidney transplantation. Similarly, the repair of renal tubular epithelial cells takes a relatively long time, resulting in delayed graft function after kidney transplantation. Renal tubular cell culture models, animal experiments and clinical studies suggest that renal tubular epithelial cell death induced by renal ischemia-reperfusion injury has two forms of necrosis and apoptosis. In the late stage, the dedifferentiated renal tubular epithelial cells proliferate, migrate and redifferentiate under the action of various repair mechanisms, and the proliferation of renal tubular epithelial cells starts gradually. As the coexistence of solid organ transplantation and ischemia-reperfusion injury, we should adopt active and effective methods to inhibit the apoptosis of renal tubular epithelial cells to the greatest extent, alleviate the adverse effects of renal ischemia-reperfusion injury, protect renal function and reduce it. The delayed recovery of graft function and the incidence of acute rejection after oligokidney transplantation can ultimately prolong the survival time of transplanted kidney and recipients, which has far-reaching clinical significance.
Sirolimus (SRL) is a mammalian target of rapamycin (mTOR) inhibitor. Animal experiments and many years of clinical application have shown that the CNI-based immunosuppressive regimen or the CNI-based immunosuppressive regimen after switching from SRL-based to sirolimus-based immunosuppressive regimens are CNI-based immunosuppressive. Compared with CNI-based immunosuppressive regimen, sirolimus significantly reduced the creeping increase of serum creatinine and improved renal function after renal transplantation. The renal function was significantly better than that of the CNI group. For patients with chronic creeping creatinine elevation and CNI nephrotoxicity after renal transplantation, timely SRL conversion therapy can significantly improve renal transplant function and prolong the survival time of renal transplant recipients.
At present, the role of SRL in ischemia-reperfusion injury is still controversial. It has been found that SRL can significantly alleviate renal ischemia-reperfusion injury and improve renal function in rats through the following mechanisms: (1) activating T cell apoptosis through indirect pathway, preventing the antigen presentation of dendritic cells (DC) and further inhibiting its maturation; (2) On Thursday, Gui et al. treated hypoxic-reoxygenated vascular endothelial cells with SRL, inhibited the adhesion of vascular endothelial cells to neutrophils by inhibiting the signal transduction pathways of ROS, JNK and NF-kappa B. Yang B et al. found that SRL interfered with renal ischemia-reperfusion injury, mainly activating. 24KDCaspase-3 can reduce the occurrence of apoptosis and the expression of Fas in distal convoluted tubules. It can protect the ischemic kidney from reperfusion injury by alleviating the immune injury induced by Fas signal pathway. Bohmova R et al. Observation of renal ischemia-reperfusion injury in transgenic hypertensive rats showed that small doses of SRL can alleviate the production of renin. In vitro, SRL inhibits the proliferation of proximal convoluted tubular cells and promotes apoptosis by inhibiting 70 kDaS6 protein kinase in renal tubular cells. In vivo, SRL inhibits tubular cell regeneration and enhances tubular fineness. Lui SL reported that SRL decreased the expression of proliferating cell nuclear antigen (PCNA) on day 1 and day 3, but on day 7 there was no difference between the control group, suggesting that SRL could aggravate renal damage mainly by inhibiting renal tubular cells. The regeneration of renal tubular cells delayed the recovery of renal function, but did not always inhibit the regeneration of renal tubular cells.
In ischemia-reperfusion injury, the effects of different doses of SRL on the proliferation and repair of renal tubular epithelial cells after ischemia-reperfusion injury and apoptosis of renal tubular epithelial cells in rats at different stages are not clear. Protective effect, however, may inhibit the proliferation, migration, redifferentiation and skeleton remodeling of renal tubular epithelial cells in the later stage as the repair procedure of renal tubular epithelial cells is initiated step by step, which may affect the recovery of renal function in a dose-dependent and reversible manner. Rat renal ischemia-reperfusion injury model was established based on the valley concentration as the early treatment concentration after renal transplantation. The expression of apoptotic gene Fas, Bcl-2 and PCNA, the expression of tubular epithelial cell repair factor HGF and BMP-7 mRNA, and the expression of NGAL, IL-18, Fas, Bcl-2 and PCNA were detected. The combined effects of perfusion injury and repair of renal tubular epithelial cells.
Part one: protective effects of sirolimus on renal ischemia-reperfusion injury in early stage
abstract
Objective: To investigate the effects of sirolimus (SRL) on renal ischemia-reperfusion injury in rats at different stages.
Method:
1. Ninety male SD rats were randomly divided into five groups: sham, I/RI/R+SRL 1mg/(kg.d), I/R+SRL 3mg/(kg.d), I/R+SRL 5mg/(kg.d).
2. a rat model of ischemia-reperfusion injury was established.
3. The corresponding dosage of SRLlmg.3mg.5mg and 10ml normal saline were given to each group 3 days before operation and daily after operation.
4.sham and I/R were given normal saline to each observation day.
5. after 1,3,7 days, 6 rats in each group were sacrificed to get whole blood and kidney tissue, and serum creatinine was detected, p2-MG.
Neutrophil gelatinase associated lipid carrier protein (NGAL) and IL-18 were measured by 6. ELISA.
7.HE staining was used to evaluate histopathological changes.
8. immunohistochemical SABC method was used to detect the expression of Fas and Bcl-2 protein in renal tissue.
9. Western-blot technology was used to detect the expression intensity of Fas and Bcl-2 protein.
10. Deoxyribonucleotide terminal transferase mediated nick end labeling (TUNEL) was used to detect the apoptosis rate of renal cells.
Result:
1. The levels of serum Cr, p2-MG, IL-18, Fas and Bcl-2, pathological score, positive expression rate of Fas and Bcl-2 protein and apoptosis index were all increased at 1 and 3 days after operation. Except for Bcl-2, I/R+SRL5 mg/(kg.d) I/R+SRL3 mg/(kg.d) I/R+SRL1 mg/(kg.d) I/R (P 0.05).
2.Bc1-2 level:][/R+SRL5mg/ (kg.d) I/R+SRL3mg/ (kg.d) I/R+SRL1mg/ (kg.d) I/Rsham (P0.05).
3. Fas, Bcl-2 level 7 days after operation: I/R+SRL5mg/ (kg.d) was different from sham and I/R+SRLlmg/ (kg.d) (P0.05).
4. The level of NGAL was higher than that of sham (P 0.05) one day after operation. The apoptosis index I/R+SRL5 mg/(kg.d) was different from the other four groups (P 0.05).
Conclusion:
1. a rat model of renal ischemia-reperfusion injury was successfully established.
2. Sirolimus can protect renal function by inhibiting apoptosis of renal tubular epithelial cells in the early stage of ischemia-reperfusion injury.
3. sirolimus dose dependently protects renal function at the early stage of ischemia-reperfusion injury.
The second part is the effect of sirolimus on the repair of rat renal tubular epithelial cells.
abstract
Objective: To investigate the effect of sirolimus (SRL) on the repair of renal tubular epithelial cells in different periods.
Method:
1. Ninety male SD (Sprague-Dawley) rats were randomly divided into five groups: sham, I/R, I/R + SRLlmg / (kg.d), I/R + SRL3mg / (kg.d), I/R + SRL5mg / (kg.d).
2. a rat model of ischemia-reperfusion injury was established.
3. Each group was given the corresponding dose of SRLlmg, 3mg, 5mg and 10ml normal saline 3 days before operation and every day after operation.
4.sham and I/R were given normal saline to each observation day.
5. after 1,3,7 days, 6 rats in each group were sacrificed to get whole blood and kidney tissues, and serum creatinine was detected.
The level of p2-MG and hepatocyte growth factor (HGF) was determined by 6. ELISA.
7.HE staining was used to evaluate histopathological changes.
8. immunohistochemical SABC method was used to detect the expression of proliferating cell nuclear antigen (PCNA) protein in renal tissue.
9. RT-PCR technology was used to detect the expression of mRNA, bone morphogenetic protein -7 (BMP-7) mRNA in repair factor HGF.
Result:
1. The levels of serum Cr, beta 2-MG and pathological score were all increased at 1 and 3 days after operation: sham I/R + SRL 5 mg / (kg.d) I/R + SRL 3 mg / (kg.d) I/R + SRL 1 mg / (kg.d) I/R (P 0.05);
2. Blood HGF value, HGF mRNA, BMP-7 mRNA level and PCNA level at 1,3,7 days after operation: shamI/R+SRL5mg/(kg.d) I/R+SRL3mg/(kg.d) I/R+SRLlmg/(kg.d) I/R (P 0.05);
No proliferating cells were found in all stages after 3.Sham.
Conclusion:
1. a rat model of ischemia-reperfusion injury was successfully established.
2. The antiproliferative effect of sirolimus on renal tubular epithelial cells in ischemia-reperfusion injury hinders the process of renal tubular epithelial cell migration and skeletal reconstruction.
3. sirolimus has a dose-dependent anti proliferative effect in ischemia-reperfusion injury.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R965

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