Effect and its mechanism of Notch1 interference on apoptosis of lung tissue of rats with chronic obstructive pulmonary disease
Objective To explore the effect of Notch1 interference on the apoptosis of lung histiocyte and the expression of apoptosis-related protein in rats with chronic obstructive pulmonary disease(COPD).Methods All the 18 male rats with SPF grade were divided into a control group,a model group,and a Notch1 interference group according to ramdom table method,with 6 rats in each group.The COPD rat model was prepared.At the day before modeling,Notch1 interfering adenovirus was injected into the tail vein of rats in the Notch1 interfering group with 1 mL 3 × 109 pfu/mL adenovirus concentrate/piece,while the control and model groups were injected with 1 mL 0.9%sodium chloride injection,respectively.HE staining was used to observe the pathological changes of rat lung tissues and semi quantitative scoring was performed.The thickness of pulmonary vascular wall was measured.Tunel staining was used to detect apoptosis in lung tissues;reactive oxygen species(ROS)detection kit was used to measure ROS levels in lung tissues;Western blot was used to determine the expressions of Notch1,B lymphoblastoma-2(Bcl-2),and Caspase-3 proteins in lung tissues.Results Compared with the model group,the semi quantitative score of lung tissues in the Notch1 interference group of rats was significantly decreased(P<0.01),and the percentage of wall thickness to outer diameter(WT)and wall area to total vascular area(WA)were both significantly decreased(both P<0.01).The apoptosis rate of Tunel staining-positive cells,the ROS level in lung tissues,and the grayscale values of Notch1 and Caspase-3 protein expressions in the Notch1 interference group were all significantly decreased(all P<0.01),while the grayscale values of Bcl-2 protein expression were significantly increased(P<0.01).Conclusion Notch1 interference can reduce apoptosis in lung tissue of COPD rats,down-regulate ROS levels,and Notch1 and Caspase-3 protein expressions,and up-regulate Bcl-2 protein expression.