The attenuation of chlorogenic acid on oxidative stress for renal injury in streptozotocin-induced diabetic nephropathy rats
The attenuation of chlorogenic acid on oxidative stress for renal injury in streptozotocin-induced diabetic nephropathy rats
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DOI：
10.1007/s12272-016-0771-3
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发表时间：
2016-06
影响因子：
6.7
通讯作者：
Han-yang Ye;Zhan-yuan Li;Yu Zheng;Yan Chen;Zhi-hong Zhou;Jian Jin
中科院分区：
文献类型：
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作者：
Han-yang Ye;Zhan-yuan Li;Yu Zheng;Yan Chen;Zhi-hong Zhou;Jian Jin
本研究旨在探讨绿原酸（CGA）对糖尿病肾病（DN）大鼠氧化应激的保护作用。CGA能显著降低DN大鼠的血糖、尿素氮和血清肌酐水平。此外，CGA显著提高了超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶的活性。此外，CGA给药后脂质过氧化丙二醛水平明显降低。免疫组化分析也显示，CGA显著下调肾组织环氧化酶-2蛋白的表达，这被认为是氧化应激的主要发病机制之一。此外，我们发现CGA可以阻断活化转录因子-6、C/EBP同源蛋白的表达，以及真核起始因子2α和双链rna活化蛋白激酶样内质网激酶的磷酸化。此外，我们试图检测糖尿病肾组织凋亡相关蛋白的存在。我们的数据提供了证据来支持CGA减轻链脲佐菌素诱导的DN大鼠的氧化应激。其分子机制可能抑制DN内质网应激反应。
The present study was undertaken to investigate whether chlorogenic acid (CGA) could protect kidney function against oxidative stress in the diabetic nephropathy (DN) rats. The treatment with CGA could decrease significantly the levels of blood glucose, blood urea nitrogen and serum creatinine in DN rats. Moreover, CGA significantly increased the activity of superoxide dismutase, glutathione peroxidase, and catalase. Moreover, the level of lipid peroxidation malondialdehyde was reduced markedly after CGA administration. Immunohistochemical analysis also showed that CGA downregulated significantly cyclooxygenase-2 protein expression in renal tissue, which is considered as one of the major pathogeneses of oxidative stress. Furthermore, we demonstrated that CGA could block the expression of activating transcription factor-6, C/EBP homology protein and the phosphorylation of eukaryotic initiation factor 2α and double stranded RNA-activated protein kinase-like endoplasmic reticulum kinase. In addition, we attempted to detect the presence of diabetic renal tissues apoptosis-related proteins. Our data provided evidence to support this fact that CGA attenuated oxidative stress in streptozocin-induced DN rats. Its molecular mechanism may inhibit the endoplasmic reticulum-stress response in DN.