Impacts of ginkgetin on ox-LDL induced vascular endothelial cell injury by regulating the TGF-β1/Smad pathway
Objective To investigate the impacts of ginkgetin on ox-LDL induced vascular endothelial cell injury by regulating the transforming growth factor-β1(TGF-β1)/Smad signaling pathway.Methods HUVEC were grouped into control group(untreated HUVEC cells),model group(HUVEC cells treated with 50 μg/mL ox-LDL),ginkgolin group(HUVEC cells treated with 50 μg/mL ox-LDL+12.5 μmol/L ginkgolin),SRI-011381 group(HU-VEC cells treated with 50 μg/mL ox-LDL+10 μmol/L TGF-β1/Smad activator SRI-011381),and ginkgetin+SRI-011381 group(HUVEC cells treated with 50 μg/mL ox-LDL+12.5 μmol/L ginkgetin+10 μmol/L SRI-011381).ELI-SA kit was applied to detect the levels of malondialdehyde(MDA),glutathione(GSH),superoxide dismutase(SOD),interleukin-6(IL-6),interleukin-1β(IL-1β)and tumor necrosis factor-α(TNF-α)in HUVEC cells;CCK-8 method was applied to detect HUVEC cell proliferation;flow cytometry was applied to detect the apoptosis rate of HUVEC cells;Western blot was applied to detect epithelial mesenchymal transition(EMT)and the expres-sion of TGF-β1/Smad pathway related proteins.Results Compared with the control group,the levels of IL-1β,IL-6,TNF-α,MDA,apoptosis rate,the protein levels of TGF-β1,Smad3,N-cadherin and Vimentin in the model group were obviously increased(P<0.05),the OD value,the levels of GSH,SOD,and the protein level of E-cad-herin were obviously reduced(P<0.05);compared with the model group,the levels of IL-1β,IL-6,TNF-α,MDA,apoptosis rate,the protein levels of TGF-β1,Smad3,N-cadherin and Vimentin in the ginkgetin group were obviously decreased(P<0.05),the A value,the levels of GSH,SOD,and the protein level of E-cadherin were obvi-ously increased(P<0.05),the trends of SRI-011381 group were opposite,SRI-011381 weakened the inhibitory ef-fect of ginkgetin on ox-LDL induced HUVEC cell damage.Conclusion Ginkgetin may improve vascular endothelial cell injury induced by ox-LDL by down-regulating the TGF-β1/Smad signaling pathway.