低浓度镉对人肾系膜细胞和肾足细胞功能的作用及机制研究
发布时间:2021-01-15 12:58
研究背景镉(cadmium,Cd)是一种常见的环境毒物和工业污染物,可通过被污染的食物、饮用水、吸烟和职业接触等途径进入人体。镉的生物半衰期较长并可以蓄积于不同靶器官,镉暴露会严重危害人体健康,它可以对骨骼、肾脏、肝脏、生殖和免疫等器官产生毒性作用,其中肾脏是镉产生危害的重要靶器官。镉可以诱导肝脏产生金属硫蛋白(Metallothionein,MT)并结合成Cd-MT,Cd-MT随血液循环转移至肾脏和其他靶器官。镉可通过应激反应损伤肾小球、近曲小管和远曲小管,在血液循环中以自由离子或和血浆蛋白结合以结合金属硫蛋白的形式存在,经肾小球滤过,可以直接损伤肾小球导致蛋白尿,镉蓄积还可以造成肾小管重吸收功能障碍。肾小球细胞主要由肾小球内皮细胞、肾系膜细胞和肾足细胞组成,我们的前期研究发现:低浓度镉对肾小球内皮细胞功能无显著影响,然而低浓度镉对肾系膜细胞和肾足细胞功能的影响尚不明确,需要进一步研究。c-Jun氨基末端激酶(JNK)家族是促分裂原活化蛋白激酶(MAPKs)成员之一,可被细胞因子、生长因子、应激等多种因素激活,参与细胞增殖与分化、细胞形态维持、细胞骨架构建等多种生物学反应。JNK被上...
【文章来源】:山东大学山东省 211工程院校 985工程院校 教育部直属院校
【文章页数】:58 页
【学位级别】:硕士
【部分图文】:
图1低浓度镉降低肾系膜细胞增殖??Figure?1.?Low?dose?Cd?decreases?proliferation?of?HRMCs:?(A)?MTT?assay?of?HRMCs??=?**
??图3??图3低浓度镉对肾系膜细胞细胞骨架F-actin影响??Figure?3.?Effects?of?low?dose?Cd?exposure?on?F-actin?arrangement?in?HRMCs.??Immunofluoresence?staining?of?F-actin?with?Phalloidin-Tetramethylrhodamine?B??isothiocyanate?in?
Figure?8.?Cd?activates?JNK?signaling?in?HRPs.?(A)?Representative?blots?of?p-JNK?and??total?JNK?from?HRPs?treated?with?4?|〇M?Cd?at?various?time-points.?GAPDH?was?used??as?a?loading?control.?Densitometric?analyses?of?(B)?p-JNK/total?JNK,?(C)?p-??JNK/GAPDH,?and?(D)?total?JNK/GAPDH.?n?=?3.?*p?<?0.05?and?**p?<?0.01?vs.?the??control?group.?Cd,?cadmium;?HRPs,?human?renal?podocytes;?JNK,?c-Jun?N-terminal??kinase;?n.s.??not?significant;?p-JNK,?phosphorylated-JNK.??
【参考文献】:
期刊论文
[1]MAPK signal pathways in the regulation of cell proliferation in mammalian cells[J]. WEI ZHANG, Hui Tu LIU The Key Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing 100875, China. Cell Research. 2002(01)
本文编号:2978913
【文章来源】:山东大学山东省 211工程院校 985工程院校 教育部直属院校
【文章页数】:58 页
【学位级别】:硕士
【部分图文】:
图1低浓度镉降低肾系膜细胞增殖??Figure?1.?Low?dose?Cd?decreases?proliferation?of?HRMCs:?(A)?MTT?assay?of?HRMCs??=?**
??图3??图3低浓度镉对肾系膜细胞细胞骨架F-actin影响??Figure?3.?Effects?of?low?dose?Cd?exposure?on?F-actin?arrangement?in?HRMCs.??Immunofluoresence?staining?of?F-actin?with?Phalloidin-Tetramethylrhodamine?B??isothiocyanate?in?
Figure?8.?Cd?activates?JNK?signaling?in?HRPs.?(A)?Representative?blots?of?p-JNK?and??total?JNK?from?HRPs?treated?with?4?|〇M?Cd?at?various?time-points.?GAPDH?was?used??as?a?loading?control.?Densitometric?analyses?of?(B)?p-JNK/total?JNK,?(C)?p-??JNK/GAPDH,?and?(D)?total?JNK/GAPDH.?n?=?3.?*p?<?0.05?and?**p?<?0.01?vs.?the??control?group.?Cd,?cadmium;?HRPs,?human?renal?podocytes;?JNK,?c-Jun?N-terminal??kinase;?n.s.??not?significant;?p-JNK,?phosphorylated-JNK.??
【参考文献】:
期刊论文
[1]MAPK signal pathways in the regulation of cell proliferation in mammalian cells[J]. WEI ZHANG, Hui Tu LIU The Key Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing 100875, China. Cell Research. 2002(01)
本文编号:2978913
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