Mechanism of Salidroside on Oxidative Stress and Apoptosis of Pulmonary Vascular Endothelial Cells in Smog-exposed Rats through NF-κB and Bcl-2 Signaling Pathways
Objective:To explore the mechanism of salidroside(SDS)on oxidative stress and apoptosis of pul-monary vascular endothelial cells in smog-exposed rats through Bcl-2,NF-κB signaling pathway.Methods:A to-tal of 60 rats were selected and divided into control group,model group,SDS 10 mg/kg,SDS 40 mg/kg,SDS 70 mg/kg,and PNS group,10 rats per group.Except for 10 rats in the control group,smoke to lung injury model was es-tablished.Rats in control group and model group were given 2 mL normal saline in gavage daily.SDS high,medi-um and low dose groups were given salidroside suspension 2 mL at 70,40 and 10 mg/kg,respectively.PNS group was given 3.6 mg/kg prednisone acetate suspension,once a day,for consecutive 21 days.Results:Compared with control group,the levels of MDA,Bax,NF-κB,p-NF-κB and apoptosis were increased in model group,while SOD and Bcl-2 were decreased(P＜0.05).Compared with model group,MDA,Bax,NF-κB,p-NF-κB and apoptosis were decreased in SDS groups,while SOD and Bcl-2 were increased(P＜0.05).There was no difference between model group and SDS 10 mg/kg group(P＞0.05),SDS 40 mg/kg group and PNS group(P＞0.05).The lung tissue of rats in control group was good.Model group had severe injury.The lung injury in each group was alleviated af-ter drug intervention.Conclusion:Salidroside can improve lung injury,oxidative stress and apoptosis of vascular endothelial cells in rats exposed to smoke,and the mechanism may be related to the regulation of Bax/Bcl-2 and NF-κB.
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维普
