Conclusions
NF-κB overexpression promotes apoptosis and inhibits cell proliferation of VSMCs. The mechanisms might be regulated by promoting FasL and HRG-1 expression.
Methods
Human aorta VSMCs were divided into control, NF-κB inhibitor, NF-κB overexpression + NF-κB inhibitor, control vector + NF-κB inhibitor, NF-κB overexpression, and control vector groups. NF-κB overexpression vector was constructed and transfected into VSMCs. Proliferation of VSMCs in each group was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide. Apoptosis of VSMCs was detected by flow cytometry. The expression of NF-κB, FasL, and hypertension-related gene (HRG-1) was measured by Western blotting.
Results
NF-κB overexpression vector was constructed correctly by restriction endonuclease, and the results showed that the activation of NF-κB could inhibit the proliferation of VSMCs. The results of flow cytometry also confirmed that NF-κB overexpression promoted apoptosis of VSMCs. Mechanically, NF-κB overexpression could up-regulate the expression of FasL and HRG-1. Conclusions: NF-κB overexpression promotes apoptosis and inhibits cell proliferation of VSMCs. The mechanisms might be regulated by promoting FasL and HRG-1 expression.