Objective To investigate whether the VEGF-A inhibitor sFLT-1 can inhibit the activation and inflammation of vascular endothelial cells, thereby reversing the renal damage in type 1 diabetic mice.
Methods Eight-week-old C57BL/6 female mice were divided into 5 weeks: healthy control group (n = 5), diabetes group (n = 5), and 15 weeks: healthy control group (n = 5), diabetes group (n = 5), the control + sFLT-1 treatment group (n = 5), the diabetes + sFLT-1 treatment group (n = 5), the type 1 diabetes model was constructed by intraperitoneal injection of streptozotocin (75 mg/kg). The treatment of sFLT-1 was started on the 6th week after modeling. Observe the pathological damage of renal tissue, the degree of macrophage infiltration, the activation degree of glomerular endothelial cells and the level of inflammation before and after sFLT-1 treatment.
Results Compared with the model group, transfection of sFLT-1 can significantly reduce the glomerular mesangial matrix content (i.e. glomerular type IV collagen level) (P<0.001), glomerular macrophage infiltration (P <0.001), glomerular endothelial cell activation (P<0.001) and glomerular tumor necrosis factor-α level (P<0.001), thereby significantly inhibiting diabetic kidney injury, and sFLT-1 in vitro It can reduce the activation of endothelial cells induced by vascular endothelial growth factor-A (P<0.001).
Conclusion sFLT-1 may reduce endothelial activation and glomerular inflammation by inhibiting VEGF-A, and ultimately reverse diabetes-related kidney damage. It is a new treatment direction for diabetic nephropathy.