Chitooligosaccharide guanidine inhibits high glucose-induced activation of DAG/PKC pathway by regulating expression of GLUT2 in type 2 diabetic nephropathy rats
Chitooligosaccharide guanidine inhibits high glucose-induced activation of DAG/PKC pathway by regulating expression of GLUT2 in type 2 diabetic nephropathy rats
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壳寡糖胍通过调节2型糖尿病肾病大鼠GLUT2表达抑制高糖诱导的DAG/PKC通路激活
DOI：
10.1016/j.jff.2017.12.032
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发表时间：
2018-02
影响因子：
5.6
通讯作者：
Liu Xiaofei
中科院分区：
文献类型：
--
作者：
Zhang Hai;Zhang Shengsheng;Wang Li;Liu Xiaofei
本实验室的前期研究表明，壳聚糖双胍盐酸盐（CSGH）和壳寡糖胍（COSG）可以通过调控葡萄糖转运蛋白（GLUTs）的表达来调控葡萄糖的摄取。在这项研究中，我们试图描述在肾脏中观察到的二酰基甘油（DAG）/蛋白激酶C-β（PKC-β）通路和GLUT 2的活化变化。STZ诱导的糖尿病大鼠通过每日灌胃给予COSG，持续8周。可见，COSG通过调节GLUT 2的过度表达和DAG的水平，显著降低空腹血糖和血糖水平。免疫组化结果显示，COSG处理后细胞内PKC-β、TGF-β等因子不同程度减少，影响细胞外基质（ECM）成分纤维连接蛋白（FN）的合成。因此，高糖诱导的DAG/PKC通路的激活被抑制，这与COSG处理通过GLUT 2的表达控制的葡萄糖浓度有关。
Previous results from our laboratory showed that chitosan biguanidine hydrochloride (CSGH) and chitooligosaccharide guanidine (COSG) could control glucose uptake by regulating the expression of glucose transporters (GLUTs) in vitro experiments. In this study, we try to delineate changes observed in activation of diacylglycerol (DAG)/protein kinase C-β(PKC-β) pathway and GLUT2 in kidney. STZ-induced diabetic rats were administered COSG via daily intra-gastric gavage for 8 weeks. Obviously, COSG significantly attenuated fasting blood glucose and blood glucose level by modulating the over-expression of GLUT2 and the level of DAG as well. Immunohistological examination revealed that factors such as PKC-βand transforming growth factor-β(TGF-β) diminished to various extents after treatment with COSG, which impinged on the synthesis of extracellular matrix (ECM) components like fibronectin (FN). As a result, high glucose-induced activation of DAG/PKC pathway is inhibited, which is associated with the concentration of glucose controlled by the expression of GLUT2 with the treatment of COSG.
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