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논문분류	춘계학술대회 초록집
제목	The protection effect of diabetic nephropathy by SAR131675 in db/db mice
저자	Seon Deok Hwang1, Joon Ho Song1, Yaeni Kim2, Ji Hee Lim2, Min Young Kim2, Eun Nim Kim2, Yu Ah Hong2, Bum Soon Choi2, Yong-Soo Kim2, Cheol Whee Park2
출판정보	2018; 2018(1):
키워드	Diabetic renal damage \| Lymhangiogenesis \| SAR131675 \| Lipotoxicity
초록	Objectives: In various renal diseases, the proliferation of lypmphatic vessels related to intrarenal fibrosis and inflammation. Recent studies also have demonstrated that accumulation of lipids in the kidney plays a crucial role in the progression of diabetic renal damage. SAR131675 is a potent and selective VEGF-R3-tyrosine kinase inhibitor and acts as a ligand for VEGF-C and VEGF-D that inhibits lymhangiogenesis. In this study, we hypothesized that SAR131675 can prevent and ameliorates lipotoxicity-induced inflammatory lymphangiogenesis in type 2 DN by inhibiting renal lymphangiogenesis Methods: Male C57BLKS/J db/m and db/db mice were fed either a regular diet chow or a diet containing SAR131675 for 12 weeks from 8 weeks of age and human proximal epithelial cells (HK2) were used. Results: SAR131475 fed db/db mice showed decreased amount of albuminuria and lipid accumulation in the kidney with no significant changes in the levels of glucose, creatinine and body weight. SAR131475 inhibited systemic inflammation and the accumulation of intrarenal triglycerides and free fatty acid, which also decreased intrarenal inflammation related to decreased chemokines and pro-inflammatory macrophage infiltration. Consistent down-regulations of VEGF-C and VEGF-R3 in the whole kidney were associated with decreased lymphatic growth, represented by LYVE-1 and podoplanin expression, tubulointerstitial fibrosis and inflammation, which were related to decreases in oxidative stress and apoptosis. With the respect to HK-2 cells, SAR131475 treatment showed favorable effects on palmitate-induced oxidative stress and apoptosis in HK-2 cells. Conclusions: Our study suggests SAR131675 as a promising therapeutic agent of DN via ameliorating renal damage by means of reduced lipotoxicity-induced inflammatory lymphangiogenesis.
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