C型钠尿肽及功能受体NPR-B对糖尿病肾病的保护作用及机制研究
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摘要
本研究以糖尿病大鼠、系膜细胞、内皮细胞为研究对象,运用酶联免疫吸附分析法、免疫组织化学及荧光技术、蛋白印迹和荧光实时定量-逆转录多聚酶链反应等多种实验方法,多方面研究C型钠尿肽(CNP)对糖尿病肾病的保护作用和机制,以及通络方剂等对CNP及NPR-B的影响。结果显示,糖尿病大鼠肾组织存在CNP及NPR-B受体的局部自调节,在糖尿病肾病的不同病理时期表达不同。通络方剂能够调节糖尿病大鼠肾皮质组织CNP及NPR-B的表达,并能促进内皮细胞CNP的合成。CNP能够通过NPR-B/cGMP途径抑制晚期糖基化终末产物或活性氧簇诱导的核因子-κB活性,并抑制系膜细胞增殖及表型转化。提示,CNP及NPR-B受体在糖尿病肾病病理过程中可能具有保护作用;通络方剂能够调节CNP和NPR-B受体表达。
This study investigated STZ-induced diabetes rats, mesangial cells and endothelial cells as object to approach the protective effection of CNP and NPR-B recptor in diabetic nephropathy and their mechanism by the method of immunohistochemistry, immunofluorescent technique, ELISA, western blot, RealTime-PCR and so on. Presence of local autogenous regulation of CNP and NPR-B were found in diabetes rats renal. CNP and NPR-B showed different characteristic on renal cortex at different pathological period, with TongLuo recipe regulated their expression. TongLuo recipe contributed to the synthesis of CNP in cultured human umbilical vein cells. CNP inhibited the active NF-κB and restrainted the proliferation and phenotype converting induced by AGEs or ROS through NPR-B/cGMP pathway in cultured mesangial cells. These study suggesting that CNP and its functional receptor NPR-B may play a protective role on diabetic nephropathy, TongLuo Recipe can regulates their express.
This study investigated STZ-induced diabetes rats, mesangial cells and endothelial cells as object to approach the protective effection of CNP and NPR-B recptor in diabetic nephropathy and their mechanism by the method of immunohistochemistry, immunofluorescent technique, ELISA, western blot, RealTime-PCR and so on. Presence of local autogenous regulation of CNP and NPR-B were found in diabetes rats renal. CNP and NPR-B showed different characteristic on renal cortex at different pathological period, with TongLuo recipe regulated their expression. TongLuo recipe contributed to the synthesis of CNP in cultured human umbilical vein cells. CNP inhibited the active NF-κB and restrainted the proliferation and phenotype converting induced by AGEs or ROS through NPR-B/cGMP pathway in cultured mesangial cells. These study suggesting that CNP and its functional receptor NPR-B may play a protective role on diabetic nephropathy, TongLuo Recipe can regulates their express.
引文
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1. Brownlee M: Biochemistry and molecular cell biology of diabetic complications. Nature. 2001 Dec 13;414(6865):813-20
2. Ha H, Yu MR, Choi YJ,et al. Role of high glucose-induced nuclear factor-kappaB activation in monocyte chemoattractant protein-1 expression by mesangial cells. J Am Soc Nephrol. 2002 Apr;13(4):894-902.
3. Thannickal VJ, Fanburg BL. Reactive oxygen species in cell signaling. Am J Physiol Lung Cell Mol Physiol. 2000 Dec;279(6):L1005-28.
4. Lin MJ, Yang XR, Cao YN, Sham JS.Hydrogen Peroxide Induced Ca2+ Mobilization in Pulmonary Arterial Smooth Muscle Cells. Am J Physiol Lung Cell Mol Physiol. 2007 Mar 16;
5. Yu JH, Kim KH, Kim H. Role of NADPH oxidase and calcium in cerulein-induced apoptosis: involvement of apoptosis-inducing factor. Ann N Y Acad Sci. 2006 Dec;1090:292-7.
6. Hajnoczky G, Csordas G, Das S, et al., Mitochondrial calcium signalling and cell death: approaches for assessing the role of mitochondrial Ca2+ uptake in apoptosis. Cell Calcium. 2006;40(5-6): 553-60.
7. Yan Y, Wei CL, Zhang WR, Cheng HP, Liu J. Related Articles, Cross-talk between calcium and reactive oxygen species signaling. Acta Pharmacol Sin. 2006; 27(7): 821-6.
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