Figures & data
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Figure 1. Cytotoxicity of Nintedanib in endothelial cells. Cells were treated with Nintedanib at concentrations of 1, 5, 10, 25, 50, 100 μM. Cell viability was determined with the CCK-8 assay (*, **, P < 0.05, 0.01 vs. Vehicle group).
![Figure 1. Cytotoxicity of Nintedanib in endothelial cells. Cells were treated with Nintedanib at concentrations of 1, 5, 10, 25, 50, 100 μM. Cell viability was determined with the CCK-8 assay (*, **, P < 0.05, 0.01 vs. Vehicle group).](/cms/asset/681b4a0f-7f15-4d7f-95f7-c42404bc795a/kbie_a_2036913_f0001_oc.jpg)
Figure 2. Nintedanib prevents ox-LDL-induced lipid accumulation in HUVECs. Cells were treated with 75 μg/mL ox-LDL with or without 10 μM and 25 μM of Nintedanib for 24 hours. (a). The levels of Total Cholesterol (TC); (b) Free Cholesterol (FC) (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).
![Figure 2. Nintedanib prevents ox-LDL-induced lipid accumulation in HUVECs. Cells were treated with 75 μg/mL ox-LDL with or without 10 μM and 25 μM of Nintedanib for 24 hours. (a). The levels of Total Cholesterol (TC); (b) Free Cholesterol (FC) (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).](/cms/asset/5110956b-d850-4be0-81ba-35b43af871fa/kbie_a_2036913_f0002_oc.jpg)
Figure 3. Nintedanib reduces ox-LDL LDL-induced inflammation in HUVECs. (a) mRNA levels of TNF-α, IL-1β, IL-6; (b) Secretion levels of TNF-α, IL-1β, IL-6 (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).
![Figure 3. Nintedanib reduces ox-LDL LDL-induced inflammation in HUVECs. (a) mRNA levels of TNF-α, IL-1β, IL-6; (b) Secretion levels of TNF-α, IL-1β, IL-6 (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).](/cms/asset/8cb0c68e-66a4-4b67-8c09-0a58a1c9df05/kbie_a_2036913_f0003_oc.jpg)
Figure 4. Nintedanib reduces ox-LDL-induced oxidative stress in HUVECs. (a) ROS levels; (b) MDA levels; (c) GSH-Px levels (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).
![Figure 4. Nintedanib reduces ox-LDL-induced oxidative stress in HUVECs. (a) ROS levels; (b) MDA levels; (c) GSH-Px levels (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).](/cms/asset/58c4f8e2-4154-4482-9384-669a5881e9b5/kbie_a_2036913_f0004_oc.jpg)
Figure 5. Nintedanib reduces ox-LDL- induced cellular senescence in HUVECs. Cells were treated with 75 μg/mL ox-LDL with or without 10 μM and 25 μM of Nintedanib for 7 days. (a). SA-β-gal staining;(b). Immunoblotting analysis of cellular senescence marker p21 andp53 (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).
![Figure 5. Nintedanib reduces ox-LDL- induced cellular senescence in HUVECs. Cells were treated with 75 μg/mL ox-LDL with or without 10 μM and 25 μM of Nintedanib for 7 days. (a). SA-β-gal staining;(b). Immunoblotting analysis of cellular senescence marker p21 andp53 (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).](/cms/asset/6980f4cd-3ff6-4d3c-b810-8d2ef70d2f3c/kbie_a_2036913_f0005_oc.jpg)
Figure 6. Nintedanib inhibits ox-LDL-induced cell cycle arrest in G0/G1 phase in HUVECs. Cell fraction in the G0/G1phase, G2/M phase, and S phase was calculated (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).
![Figure 6. Nintedanib inhibits ox-LDL-induced cell cycle arrest in G0/G1 phase in HUVECs. Cell fraction in the G0/G1phase, G2/M phase, and S phase was calculated (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).](/cms/asset/ad25a7c0-d3fa-4f09-a0c8-06c47df35bdb/kbie_a_2036913_f0006_oc.jpg)
Figure 7. Nintedanib inhibits the expression of Arg-II elevated by ox-LDL treatment in HUVECs. Cells were treated with 75 μg/mL ox-LDL with or without 10 μM and 25 μM of Nintedanib for 24 hours. (a). mRNA of Arg-II; (b). protein level of Arg-II (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).
![Figure 7. Nintedanib inhibits the expression of Arg-II elevated by ox-LDL treatment in HUVECs. Cells were treated with 75 μg/mL ox-LDL with or without 10 μM and 25 μM of Nintedanib for 24 hours. (a). mRNA of Arg-II; (b). protein level of Arg-II (***, P < 0.001 vs. Vehicle group; #, ##, P < 0.05, 0.01 vs. ox-LDL group).](/cms/asset/e9865531-d840-44ea-9fe6-6337ef74040e/kbie_a_2036913_f0007_oc.jpg)
Figure 8. Overexpression of Arg-II blocked the protective effects of Nintedanib on ox-LDL induced and cellular senescence. Cells were infected with Arg-II lentivirus for 48 hours and then treated with 75 μg/mL ox-LDL with or without 25 μM of Nintedanib for 24 hours. (a). Western blot analysis revealed successful overexpression of Arg-II; (b). Immunoblotting analysis of cellular senescence markerp21 andp53;(c). SA-β-gal staining (***, P < 0.001 vs. Vehicle group; ##, P < 0.01 vs. ox-LDL group; $$$, P < .001 vs. ox-LDL+Nintedanib group).
![Figure 8. Overexpression of Arg-II blocked the protective effects of Nintedanib on ox-LDL induced and cellular senescence. Cells were infected with Arg-II lentivirus for 48 hours and then treated with 75 μg/mL ox-LDL with or without 25 μM of Nintedanib for 24 hours. (a). Western blot analysis revealed successful overexpression of Arg-II; (b). Immunoblotting analysis of cellular senescence markerp21 andp53;(c). SA-β-gal staining (***, P < 0.001 vs. Vehicle group; ##, P < 0.01 vs. ox-LDL group; $$$, P < .001 vs. ox-LDL+Nintedanib group).](/cms/asset/f2e44787-4485-4cff-87c2-2bbb4aabe105/kbie_a_2036913_f0008_oc.jpg)
Data availability statement /Availability of data materials
The data and materials of this study are available upon reasonable request from the corresponding authors.