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Nod2 silencing is involved in the protective role of Calycosin in diabetic nephropathy cell model

Di Huang, Peicheng Shen, Chen Wang, Jiandong Gao, Chaoyang Ye, Feng Wu


Diabetic nephropathy (DN) is considered as the most serious diabetic microvascular complication. Podocyte injury has a crucial role in the pathogenesis of DN. Calycosin, a major active component of a Traditional Chinese Medicine (TCM), has been found to play a protective role in DN. However, the mechanism has not been well discovered. In this study, high D-Glucose (D-Glu) was used to treat podocytes to establish podocyte DN cell model. DCFH-DA probe and annexin V/PI staining kit were used to detect Reactive Oxygen Species (ROS) level and cell apoptosis, respectively. Firstly, Nod2 expression level was upregulated after treatment with D-Glu. Then, D-Glu induced cell apoptosis and production of ROS, but Calycosin and Nod2 silencing alleviated these effects. Further, the decrease of nephrin and podocalyxin induced by D-Glu could be blocked by Calycosin and Nod2 silencing. Increase protein level of p-p38 induced by D-Glu was ameliorated by Calycosin and Nod2 silencing. In addition, Nod2 overexpression enhanced the apoptosis rates, the production of ROS, and the protein level of p-p38, but these effects were ameliorated by Calycosin. In conclusion, knockdown of Nod2 participated in the protection of Calycosin in D-Glu induced DN cell model via p38-MAPK signaling.


Calycosin, Nod2, DN, p38.

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