Mechanism by which Notch1 interference regulates the apoptosis of pulmonary microvascular endothelial cells / 中国基层医药

ABSTRACT

Objective:To investigate the mechanism of how Notch1 interference regulates the apoptosis of pulmonary vascular endothelial cells.Methods:During January to December 2022, human pulmonary microvascular endothelial cells were transfected with Notch1 siRNA, and the cell viability in each group was evaluated using the Cell Counting Kit-8 assay. The level of reactive oxygen species was determined using flow cytometry, while cell apoptosis was assessed using the same technique. After treatment with Notch1 siRNA, the protein expression levels of Notch1, Bcl-2, and Caspase-3 in the human pulmonary microvascular endothelial cells were detected using western blot assay.Results:The expression level of Notch1 mRNA in human pulmonary microvascular endothelial cells was significantly lower in the blank control and si-Notch1 groups than that in the siNC group ( t = 11.25, 9.47, both P < 0.05). Additionally, the optical density value and Bcl-2 protein expression level in the lipopolysaccharide (LPS) + Notch1 siRNA group were significantly higher than those in the LPS and LPS + siRNA groups ( t = 11.26, 11.68, both P < 0.05). The level of reactive oxygen species and the apoptosis rate of cells were significantly lower in the LPS + Notch1 siRNA group compared with the LPS and LPS + siRNA groups ( t = 11.68, 11.87, both P < 0.05). Furthermore, the protein expression levels of Notch1 and Caspase-3 were also significantly lower in the LPS + Notch1 siRNA group compared with the LPS and LPS + siRNA groups ( t = 5.08, 6.60, 3.84, 5.83, all P < 0.05). Conclusion:Notch1 interference may interference in the apoptosis of human pulmonary microvascular endothelial cells through regulating the level of reactive oxygen species, downregulating the protein expression of Notch1 and Caspase-3, and upregulating the protein expression of Bcl-2. These actions may contribute to the treatment of chronic obstructive pulmonary disease.