红景天苷调控NF-κB、Bcl-2信号通路对烟雾暴露大鼠氧化应激及肺血管内皮细胞凋亡的影响  

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

作　　者：粟治胜 王晓江[2] 李正 刘东[2] Su Zhisheng;Wang Xiaojiang;Li Zheng;Liu Dong(Jiulongpo District People′s Hospital,Chongqing 400050,China)

机构地区：[1]重庆市九龙坡区人民医院,重庆400050 [2]重庆医科大学附属第一医院,重庆400016

出　　处：《中国中医急症》2024年第3期434-438,共5页Journal of Emergency in Traditional Chinese Medicine

基　　金：西南医科大学校级基金资助项目(2017-ZRQN-076)。

摘　　要：目的探究红景天苷(SDS)通过调控B淋巴细胞瘤-2(Bcl-2)、核转录因子-κB(NF-κB)信号通路对烟雾暴露大鼠氧化应激及肺血管内皮细胞凋亡的机制。方法选取60只大鼠分为对照组、模型组、SDS 10 mg/kg、SDS 40 mg/kg、SDS 70 mg/kg、醋酸泼尼松(PNS)组,每组10只,除对照组外,其余均建立烟雾致肺损伤模型,对照组与模型组大鼠每日采用等量生理盐水灌胃;SDS高、中、低剂量组分别按70、40、10 mg/kg剂量给予SDS混悬液2 mL灌胃;PNS组给予PNS混悬液3.6 mg/kg灌胃,均每日1次,连续21 d。结果与对照组比较,模型组大鼠血清中丙二醛(MDA)、Bcl-2相关X因子(Bax)、NF-κB、p-NF-κB及细胞凋亡升高,超氧化物歧化酶(SOD)、Bcl-2降低(P<0.05);与模型组比较,SDS各剂量组MDA、Bax、NF-κB、p-NF-κB及细胞凋亡均有所降低,SOD、Bcl-2也有所升高(P<0.05),且模型组与SDS 10 mg/kg组比较无明显差异(P>0.05),SDS 40 mg/kg组与PNS组比较无明显差异(P>0.05)。对照组大鼠肺组织良好;模型组肺损伤严重;药物干预后各组肺损伤均减轻。结论SDS可改善烟雾暴露大鼠肺损伤、氧化应激及血管内皮细胞凋亡,其机制可能与调控Bax/Bcl-2及NF-κB相关。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.

关 键 词：烟雾暴露 红景天苷 肺血管内皮细胞 BCL-2 NF-ΚB 氧化应激 大鼠 

分 类 号：R285.5[医药卫生—中药学]