【摘要】：鎘是環(huán)境中常見的高毒性重金屬污染物,急性或慢性鎘暴露能引起多種器官和組織的損傷。近年來,由于工業(yè)生產(chǎn)中鎘生產(chǎn)量和使用量的激增及相關(guān)工業(yè)廢物帶來的污染加重,使得環(huán)境中鎘含量呈快速上升趨勢;鎘在環(huán)境中的半衰期長達(dá)10-30年,進(jìn)入環(huán)境后不能像有機(jī)污染物一樣被微生物降解,并且可以通過食物鏈效應(yīng)最終蓄積在人體中。因此,鎘暴露給公眾健康帶來的危害引起了廣泛關(guān)注。腎臟是鎘毒性作用的靶器官,國內(nèi)外學(xué)者從環(huán)境污染、職業(yè)性暴露和動物試驗(yàn)等多等方面對鎘所致腎毒性機(jī)理進(jìn)行了廣泛、深入地研究;但這些研究多集中于凋亡機(jī)理的探究,而對鎘所致腎臟毒性過程中自噬的機(jī)理、作用及其與凋亡關(guān)系的探究較少。1.鎘誘導(dǎo)大鼠腎臟皮質(zhì)和腎小管上皮細(xì)胞發(fā)生自噬分為體外和體內(nèi)兩部分。體外試驗(yàn)采用機(jī)械篩網(wǎng)結(jié)合酶消化法建立原代大鼠腎小管上皮細(xì)胞(rPT cells)培養(yǎng)模型,在傳一代細(xì)胞增殖活性最強(qiáng)時間進(jìn)行鎘染毒處理,同時選擇NRK-52E細(xì)胞株進(jìn)行同樣處理。CCK-8法測定不同濃度的鎘在不同染毒時間對rPT細(xì)胞和NRK-52E細(xì)胞活性的影響;MDC熒光探針法檢測不同濃度的鎘在不同染毒時間對rPT細(xì)胞和NRK-52E細(xì)胞自噬水平的影響;2.5 μ和5 μM鎘處理rPT細(xì)胞、5 ⒚M和10 μM鎘處理NRK-52E細(xì)胞6 h,免疫印跡法檢測自噬相關(guān)蛋白LC3Ⅱ、p62和Beclin-1表達(dá)水平變化。結(jié)果表明,2.5 μM和5 μM鎘處理rPT細(xì)胞、5 μM和10μ 鎘處理NRK-52E細(xì)胞6h,細(xì)胞活性最強(qiáng),自噬水平最高,極顯著高于對照組(P0.01);2.5μM和5μM鎘處理rPT細(xì)胞、5μM和10μM鎘處理NRK-52E細(xì)胞12h,細(xì)胞自噬水平最低,極顯著低于對照組(P0.01)。體內(nèi)試驗(yàn)選擇SD大鼠32只,隨機(jī)分為4組:對照組(DDW)和鎘組(CdAc2,50mg/kg·bw),飼養(yǎng)1周;對照組(DDW)和鎘組(CdAc2,50mg/kg·bw),飼養(yǎng)8周。取腎臟皮質(zhì),RT-PCR法檢測自噬相關(guān)基因LC3、p62和Beclin-1表達(dá)量變化;免疫印跡法檢測自噬相關(guān)蛋白LC3Ⅱ、p62和Beclin-1表達(dá)水平變化。結(jié)果表明,鎘染毒處理1周后,大鼠腎臟皮質(zhì)自噬水平極顯著高于對照組(P0.01);與對照組相比Beclin-1表達(dá)水平極顯著升高(P0.01)。鎘染毒處理8周,大鼠腎臟皮質(zhì)自噬水平極顯著低于對照組(P0.01)。體外和體內(nèi)研究表明,低劑量鎘短時間處理可以誘導(dǎo)腎臟皮質(zhì)和腎小管上皮細(xì)胞發(fā)生自噬,而長時間處理則抑制自噬。2.鎘誘導(dǎo)大鼠腎臟皮質(zhì)和腎小管上皮細(xì)胞發(fā)生凋亡分為體外和體內(nèi)兩部分。體外試驗(yàn)采用機(jī)械篩網(wǎng)結(jié)合酶消化法建立原代大鼠腎小管上皮細(xì)胞(rPT cells)培養(yǎng)模型,在傳一代細(xì)胞增殖活性最強(qiáng)時間進(jìn)行鎘染毒處理,同時選擇NRK-52E細(xì)胞株進(jìn)行同樣處理。DAPI染色法檢測不同濃度的鎘在不同染毒時間對rPT細(xì)胞和NRK-52E細(xì)胞凋亡的影響;流式細(xì)胞術(shù)檢測2.5 μM和5μ 鎘處理rPT細(xì)胞、5(μM和10 μM鎘處理NRK-52E細(xì)胞12 h,細(xì)胞凋亡率變化;免疫印跡法檢測2.5 μM和5 μM鎘處理rPT細(xì)胞、5 μM和10 μM鎘處理NRK-52E細(xì)胞12 h,線粒體凋亡途徑相關(guān)蛋白Cyt C、Cleaved caspase-9和Cleaved caspase-3表達(dá)水平變化,內(nèi)質(zhì)網(wǎng)凋亡途徑相關(guān)蛋白ATF-6、GRP78、IRE1α和Cleavedcaspase-12表達(dá)水平變化,Fas/FasL凋亡途徑相關(guān)蛋白Fas、FasL、FADD、Cleavedcaspase-8表達(dá)水平變化。結(jié)果表明,2.5μM和5μM鎘處理rPT細(xì)胞、5μM和10μM鎘處理NRK-52E細(xì)胞6h,細(xì)胞凋亡率最低(P0.01),6h之后凋亡率開始升高,12h細(xì)胞凋亡率最高(P0.01);2.5μM和5μM鎘處理rPT細(xì)胞、5μM和10 μM鎘處理NRK-52E細(xì)胞12 h,與對照組相比,線粒體凋亡途徑、內(nèi)質(zhì)網(wǎng)凋亡途徑、Fas/FasL凋亡途徑相關(guān)蛋白表達(dá)水平都顯著或極顯著升高(P0.05或P0.01)。體內(nèi)試驗(yàn)選擇SD大鼠32只,隨機(jī)分為4組:對照組(DDW)和鎘組(CdAc2,50 mg/kg·bw),飼養(yǎng)1周;對照組(DDW)和鎘組(CdAc2,50mg/kg·bw),飼養(yǎng)8周。飼養(yǎng)1周后取腎臟皮質(zhì),RT-PCR法檢測凋亡基因Caspase-3表達(dá)量變化;免疫印跡法檢測凋亡蛋白Cleaved caspase-3表達(dá)水平變化。飼養(yǎng)8周后取腎臟皮質(zhì),RT-PCR法檢測線粒體凋亡途徑相關(guān)基因Cyt C、Caspase-9和Caspase-3表達(dá)量變化,內(nèi)質(zhì)網(wǎng)凋亡途徑相關(guān)基因ATF-6、GRP78、IRE1α和 Caspase-12 表達(dá)量變化,Fas/FasL 凋亡途徑相關(guān)基因 Fas、FasL、FADD、Caspase-8表達(dá)量變化;線粒體凋亡途徑相關(guān)蛋白Cyt C、Cleaved caspase-9和Cleaved caspase-3表達(dá)水平變化,內(nèi)質(zhì)網(wǎng)凋亡途徑相關(guān)蛋白ATF-6、GRP78、IRE1α和Cleaved caspase-12 表達(dá)水平變化,Fas/FasL 凋亡途徑相關(guān)蛋白 Fas、FasL、FADD、Cleaved caspase-8表達(dá)水平變化。結(jié)果表明,鎘染毒處理1周,與對照組相比,大鼠腎臟皮質(zhì)細(xì)胞凋亡無顯著變化(P0.05);鎘染毒處理8周,與對照組相比,線粒體凋亡途徑、內(nèi)質(zhì)網(wǎng)凋亡途徑、Fas/FasL凋亡途徑相關(guān)基因和蛋白表達(dá)水平都顯著或極顯著升高(P0.05或P0.01)。體外和體內(nèi)研究表明,低劑量鎘短時間處理激活細(xì)胞的保護(hù)機(jī)制,減少細(xì)胞凋亡,而長時間處理則同時激活線粒體凋亡途徑、內(nèi)質(zhì)網(wǎng)凋亡途徑和Fas/FasL凋亡途徑,誘導(dǎo)細(xì)胞發(fā)生凋亡。3.鎘誘導(dǎo)細(xì)胞自噬與細(xì)胞凋亡的關(guān)系采用機(jī)械篩網(wǎng)結(jié)合酶消化法建立原代大鼠腎小管上皮細(xì)胞(rPT cells)培養(yǎng)模型,在傳一代細(xì)胞增殖活性最強(qiáng)時間進(jìn)行處理。流式細(xì)胞術(shù)檢測自噬抑制劑3-MA對鎘處理rPT細(xì)胞6h凋亡率的影響、自噬激活劑RAPA對鎘處理rPT細(xì)胞12h凋亡率的影響;免疫共沉淀法檢測2.5 μM和5 μM鎘處理rPT細(xì)胞6 h,Beclin-1與線粒體凋亡途徑相關(guān)蛋白Cyt C、Caspase-3、Cleaved caspase-3、Caspase-9、Cleaved caspase-9、Bcl-2、Bax,與內(nèi)質(zhì)網(wǎng)凋亡途徑相關(guān)蛋白 ATF-6、GRP78、IRE1α、Caspase-12、Cleavedcaspase-12 及 Fas/FasL 凋亡途徑相關(guān)蛋白Fas、FasL、FADD、Caspase-8、Cleavedcaspase-8的相互作用;免疫印跡法檢測Beclin-1敲減對鎘誘導(dǎo)的自噬和凋亡的影響;DCFH-DA探針法檢測鎘誘導(dǎo)ROS生成量的變化;透射電子顯微鏡檢測包裹線粒體的溶酶體數(shù)量變化。結(jié)果表明,自噬抑制劑3-MA極顯著促進(jìn)鎘誘導(dǎo)rPT細(xì)胞凋亡(P0.01),同時自噬激活劑RAPA極顯著抑制鎘誘導(dǎo)rPT細(xì)胞凋亡(P0.01);2.5 μM和5 μM鎘處理rPT細(xì)胞6 h,Beclin-1與線粒體凋亡途徑相關(guān)蛋白CytCcyto、Caspase-9、Caspase-3、Baxmito,與內(nèi)質(zhì)網(wǎng)凋亡途徑相關(guān)蛋白Caspase-12,與Fas/FasL凋亡途徑相關(guān)蛋白Cleaved caspase-8存在明顯相互作用,與Bcl-2Totai和Bcl-2Mito也存在明顯相互作用,但呈負(fù)相關(guān)劑量效應(yīng)關(guān)系,與其他蛋白不存在或僅存在極微弱相互作用;Beclin-1敲減導(dǎo)致LC3Ⅱ蛋白表達(dá)極顯著下降(P0.01),p62蛋白表達(dá)極顯著升高(P0.01),Cleavedcaspase-12、Cleavedcaspase-8、Cleavedcaspase-3表達(dá)極顯著升高(P0.01);2.5 μM Cd和5 μM Cd處理rPT細(xì)胞6 h,5 μM鎘組與2.5 μM鎘組相比,ROS 水平顯著降低(P0.05),包裹線粒體的溶酶體數(shù)量顯著增多(PP0.05)。說明,自噬在鎘誘導(dǎo)rPT細(xì)胞凋亡過程中通過Beclin-1發(fā)揮保護(hù)作用,同時通過清除受損線粒體、降低ROS水平發(fā)揮保護(hù)作用。
[Abstract]:Cadmium is a common high toxic heavy metal pollutant in the environment. Acute or chronic cadmium exposure can cause a variety of organs and tissue damage. In recent years, the cadmium content in the environment is rising rapidly because of the increase of cadmium production and use and the pollution caused by industrial wastes in industrial production. The half-life of cadmium in the environment is long. For 10-30 years, after entering the environment, it can not be degraded by microorganisms like organic pollutants and can eventually be stored in the human body through the food chain effect. Therefore, the harm caused by cadmium exposure to public health has attracted wide attention. The kidney is the target organ of the toxic effect of cadmium, and the domestic and foreign scholars from the environmental pollution, occupational exposure and animal test. The mechanism of renal toxicity induced by cadmium is extensively studied in many aspects, but these studies focus on the mechanism of apoptosis, and the mechanism of autophagy, the role of autophagy and the relationship with apoptosis in renal toxicity induced by cadmium are less.1. induced autophagy in the renal cortex and tubular epithelial cells of rats induced by cadmium in vitro And in the two part of the body. In vitro, the primary rat renal tubular epithelial cell (rPT cells) culture model was established by mechanical screening and enzyme digestion. In the strongest time of the first generation, the cell proliferation activity was treated with cadmium. At the same time, the NRK-52E cell line was selected for the same treatment.CCK-8 method to determine the different concentration of cadmium in different time to rP The effect of T cell and NRK-52E cell activity, MDC fluorescence probe was used to detect the effect of cadmium on the autophagy level of rPT cells and NRK-52E cells at different time of exposure. 2.5 Mu and 5 mu M cadmium treated rPT cells, 5 M and 10 micron cadmium treatment NRK-52E cells 6 h. The results showed that 2.5 M and 5 M cadmium treated rPT cells, 5 mu M and 10 mu cadmium treated NRK-52E cell 6h, the cell activity was the strongest, the level of autophagy was the highest, which was significantly higher than that of the control group (P0.01); 2.5 mu M and 5 micron cadmium treated rPT cells, 5 mu M and 10 micron cadmium treated cells, the level of autophagy was the lowest, significantly lower than the control group. 32 SD rats were randomly divided into 4 groups: the control group (DDW) and the cadmium group (CdAc2,50mg/kg. BW) for 1 weeks; the control group (DDW) and the cadmium group (CdAc2,50mg/kg. BW) were reared for 8 weeks. The renal cortex was taken to detect the expression of autophagy related genes LC3, p62 and Beclin-1, and the immunoblotting was used to detect the autophagy related protein LC3 II. The results showed that the autophagy level of renal cortex in rats was significantly higher than that of the control group (P0.01) after 1 weeks of cadmium treatment, and the expression level of Beclin-1 was significantly higher than that of the control group (P0.01). The autophagy level of renal cortex in rats was significantly lower than that of the control group (P0.01). In vitro and in vivo studies showed that low dose of cadmium in vitro and in vivo Time treatment can induce autophagy in renal cortex and renal tubular epithelial cells, while long time treatment inhibits the apoptosis of renal cortical and tubular epithelial cells of.2. induced by autophagy into two parts in vitro and in vivo. In vitro, the primary rat renal tubular epithelial cells (rPT cell) were established by mechanical sieve binding enzyme digestion method (rPT). S) culture model, cadmium treatment at the strongest time of cell proliferation in the first generation, and the effect of NRK-52E cell line on the same treatment.DAPI staining method to detect the apoptosis of rPT cells and NRK-52E cells at different concentration of cadmium at different time of exposure; the flow cytometry was used to test 2.5 mu M and 5 micron cadmium to treat rPT cells, 5 (mu M and 10 um M cadmium). The apoptosis rate of NRK-52E cells was 12 h and the rate of apoptosis was changed; rPT cells treated with 2.5 and 5 M were detected by Western blot and 12 h in NRK-52E cells treated with cadmium and 10 micron M. The apoptotic pathway related protein Cyt C, the apoptosis pathway related protein of the endoplasmic reticulum, and the apoptosis pathway related protein of the endoplasmic reticulum The expression level of aspase-12 expression, Fas/FasL apoptosis pathway related protein Fas, FasL, FADD, Cleavedcaspase-8 expression level changes. The results showed that 2.5 mu M and 5 mu M treated rPT cells, 5 mu M and 10 mu M cadmium treatment NRK-52E cells, the apoptosis rate began to rise, the apoptosis rate was the highest, 2.5 Mu and 5 mu cadmium cadmium. Treatment of rPT cells, 5 mu M and 10 u M cadmium treated NRK-52E cells 12 h. Compared with the control group, the mitochondrial apoptosis pathway, the apoptosis pathway of endoplasmic reticulum, and the expression level of Fas/FasL apoptosis pathway related proteins were significantly or significantly increased (P0.05 or P0.01). In vivo, 32 rats were randomly divided into 4 groups: control group (DDW) and cadmium group (CdAc2,50 mg/kg. For 1 weeks, the control group (DDW) and the cadmium group (CdAc2,50mg/kg BW) were reared for 8 weeks. After 1 weeks of feeding, the renal cortex was taken and the Caspase-3 expression of apoptosis gene was detected by RT-PCR method. The expression of Cleaved caspase-3 expression of apoptotic protein was detected by Western blot. After 8 weeks, the renal cortex was taken and RT-PCR method was used to detect the Cyt C of the mitochondrial apoptotic pathway related genes and C. C Changes in the expression of aspase-9 and Caspase-3, the changes in the expression of ATF-6, GRP78, IRE1, and Caspase-12 of the apoptosis pathway related genes of the endoplasmic reticulum, Fas/FasL apoptosis pathway related genes Fas, FasL, FADD, Caspase-8 expression. The expression levels of ATF-6, GRP78, IRE1, and Cleaved caspase-12, the expression level of Fas/FasL apoptosis pathway related proteins Fas, FasL, FADD, Cleaved caspase-8 were changed. The results showed that there was no significant change in renal cortical cell apoptosis (P0.05) with the control group for 1 weeks, compared with the control group (P0.05); cadmium treatment for 8 weeks, and control. Compared with the group, the apoptosis pathway of mitochondria, the apoptosis pathway of endoplasmic reticulum, and the level of Fas/FasL apoptosis pathway related genes and protein expression were significantly or significantly increased (P0.05 or P0.01). In vitro and in vivo, the study in vitro and in vivo showed that low dose cadmium was used for short time treatment to activate cell protection mechanism and reduce cell apoptosis, while long time treatment simultaneously activated mitochondria withering. The pathway of death, the apoptosis pathway of endoplasmic reticulum and the apoptosis pathway of Fas/FasL, inducing cell apoptosis and.3. cadmium induced autophagy to induce cell autophagy and cell apoptosis, the primary rat renal tubular epithelial cell (rPT cells) culture model was established by mechanical sieve binding enzyme digestion method, and the best time for cell proliferation in the first generation was processed. Flow cytometry The effect of autophagy inhibitor 3-MA on the apoptosis rate of 6h in rPT cells treated with cadmium, the effect of autophagy activator RAPA on the apoptosis rate of 12h in rPT cells treated with cadmium; the immunocoprecipitation method was used to detect the rPT cell 6 h of 2.5 mu M and 5 micron M, and Beclin-1 and mitochondrial apoptosis pathway related proteins Cyt. Bax, the interaction of ATF-6, GRP78, IRE1 alpha, Caspase-12, Cleavedcaspase-12 and Fas/FasL apoptosis pathway related protein Fas, FasL, FADD, Caspase-8, Cleavedcaspase-8, and immunoblotting to detect the effect of cadmium induced autophagy and apoptosis The changes in the amount of the lysosomes were detected by transmission electron microscopy. The results showed that the autophagy inhibitor 3-MA significantly promoted the apoptosis of rPT cells (P0.01) induced by cadmium, while the autophagy activator RAPA significantly inhibited the apoptosis of rPT cells induced by cadmium (P0.01); 2.5 mu M and 5 u M treated rPT cell 6 h, Beclin-1 and mitochondrial apoptosis Diameter related proteins CytCcyto, Caspase-9, Caspase-3, Baxmito, and the apoptosis pathway related protein Caspase-12 of endoplasmic reticulum, which interact with Fas/FasL apoptotic pathway related protein Cleaved caspase-8, and have obvious interaction with Bcl-2Totai and Bcl-2Mito, but there is a negative correlation of dose effect, which does not exist or exists only with other proteins. The expression of LC3 II protein decreased significantly (P0.01), the expression of p62 protein increased significantly (P0.01), the expression of Cleavedcaspase-12, Cleavedcaspase-8 and Cleavedcaspase-3 increased significantly (P0.01), and the 2.5 mu M Cd and 5 micron M cells treated 6 cells, and 5 mu cadmium group was significantly lower than the 2.5 micron cadmium group. 0.05) the number of lysosomes in the parcel mitochondria increased significantly (PP0.05). It shows that autophagy plays a protective role through Beclin-1 during the apoptosis of rPT cells induced by cadmium, and plays a protective role by removing the damaged mitochondria and reducing the level of ROS.
【學(xué)位授予單位】：揚(yáng)州大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2017
【分類號】：R114

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