首页|银杏素调节TGF-β1/Smad通路对ox-LDL诱导血管内皮细胞损伤的影响

银杏素调节TGF-β1/Smad通路对ox-LDL诱导血管内皮细胞损伤的影响

扫码查看
目的 探讨银杏素调节转化生长因子-β1(TGF-β1)/Smad信号通路对ox-LDL诱导血管内皮细胞损伤的影响.方法 将人脐静脉血管内皮细胞HUVEC分为对照组(未处理的HUVEC细胞)、模型组(50μg/mL ox-LDL 处理的 HUVEC 细胞)、银杏素组(50 μg/mL ox-LDL+12.5 μmol/L 银杏素处理 HUVEC 细胞)、SRI-011381 组(50 μg/mL ox-LDL+10 μmol/L 的 TGF-β1/Smad 激活剂 SRI-011381 处理 HUVEC 细胞)、银杏素+SRI-011381 组(50 μg/mL ox-LDL+12.5 μmol/L 银杏素+10 μmol/L 的 SRI-011381 共同处理 HUVEC 细胞).ELISA试剂盒检测HUVEC细胞丙二醛(MDA)、谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、IL-6、IL-1β、TNF-α水平;CCK-8法检测HUVEC细胞增殖;流式细胞术检测HUVEC细胞凋亡率;Western blot检测细胞上皮间质转化(EMT)、TGF-β1/Smad通路相关蛋白表达.结果 与对照组相比,模型组IL-1β、IL-6、TNF-α、MDA水平、细胞凋亡率、TGF-β1、Smad3、神经型钙黏附蛋白(N-cadherin)、波形蛋白(Vimentin)蛋白水平显著增加(P<0.05),A值、GSH、SOD水平、上皮钙黏附素(E-cadherin)蛋白水平显著降低(P<0.05);与模型组相比,银杏素组IL-1β、IL-6、TNF-α、MDA水平、细胞凋亡率、TGF-β1、Smad3、N-cadherin、Vimentin蛋白水平显著下降(P<0.05),A值、GSH、SOD水平、E-cadherin蛋白水平显著升高(P<0.05),而SRI-011381组趋势相反,SRI-011381减弱了银杏素对ox-LDL诱导的HUVEC细胞损伤的抑制作用.结论 银杏素可能通过下调TGF-β1/Smad信号通路对ox-LDL诱导的血管内皮细胞损伤起到改善作用.
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.

GinkgetinTGF-β1/Smad signaling pathwayOxidized low-density lipoprotein(ox-LDL)Vascular endothelial cellsOxidative damage

李贺、曹慧、冯莉莉

展开 >

湖南省脑科医院心内科,湖南长沙 410007

银杏素 TGF-β1/Smad信号通路 氧化低密度脂蛋白 血管内皮细胞 氧化损伤

湖南省自然科学基金

2019JJ80026

2024

解剖学研究
广东省解剖学会 中国解剖学会

解剖学研究

CSTPCD
影响因子:0.327
ISSN:1671-0770
年,卷(期):2024.46(1)
  • 24