摘要
目的:探讨桔梗皂苷D对脂多糖诱导的大鼠急性肺损伤的保护作用及其机制。方法:将42只雄性SPF级SD大鼠随机分为假手术组、桔梗皂苷D对照组、模型组、低剂量桔梗皂苷D组、高剂量桔梗皂苷D组和地塞米松组,每组7只。除假手术组和桔梗皂苷D对照组外,其余各组以气道滴注脂多糖诱导大鼠急性肺损伤模型。观察造模前后大鼠一般情况。造模24 h后,腹主动脉采血并分离血清,剖胸取肺,测定右肺湿/干重比;HE染色法观察肺组织病理变化;ELISA检测血清白细胞介素1β(IL-1β)、IL-18、IL-6和肿瘤坏死因子α(TNF-α)水平;试剂盒检测大鼠血清丙二醛(MDA)、髓过氧化物酶(MPO)、过氧化氢酶(CAT)、微量还原型谷胱甘肽(GSH)和谷胱甘肽过氧化物酶(GSH-Px)水平;Western blot检测核因子κB(NF-κB)p65、p-p65、IκB和p-IκB蛋白水平。结果:与假手术组比较,模型组大鼠肺组织病理变化呈典型的急性炎症改变,肺组织损伤明显;肺湿/干重比,血清IL-1β、IL-18、TNF-α和IL-6含量,血清MDA含量和MPO活性,以及肺组织NF-κB蛋白表达显著升高(P<0.01);血清CAT、GSH和GSH-Px活性显著降低(P<0.01)。与模型组比较,低、高剂量桔梗皂苷D组及地塞米松组肺组织病理损伤均有不同程度的减轻;肺湿/干重比,血清IL-1β、IL-18、TNF-α和IL-6含量,血清MDA含量及MPO活性,以及肺组织NF-κB蛋白表达均显著降低(P<0.05或P<0.01);血清CAT、GSH和GSH-Px活性显著升高(P<0.05或P<0.01)。结论:桔梗皂苷D预处理可显著减轻脂多糖诱导的急性肺损伤大鼠肺组织的病理损害,其机制可能是通过NF-κB信号转导通路抑制细胞因子IL-1β、IL-18、TNF-α和IL-6分泌,抑制氧化应激反应,保护肺组织,减轻肺水肿。
AIM:To study the protective effect of platycodin D(PLD)on rats with lipopolysaccharide(LPS)-induced acute lung injury(ALI)and its possible mechanism.METHODS:Forty-two male Sprague-Dawley rats were randomly divided into six groups(n=7):sham operation(sham)group,PLD control(PLD)group,model group,low-dose PLD(PLD-L)group,high-dose PLD(PLD-H)group and dexamethasone(Dex)group.All rats were given LPS to induce the rat ALI model except those in sham and PLD groups.Serum and lung tissue samples were harvested after treatment with LPS for 24 h.Wet to dry weight(W/D)ratio of the lung was recorded.Hematoxylin-eosin(HE)staining was used to observe the pathological changes of lung tissues.The serum levels of interleukin(IL)-1β,IL-18,IL-6,tumor necrosis factor-α(TNF-α),malondialdehyde(MDA),myeloperoxidase(MPO),catalase(CAT),glutathione(GSH)and glutathione peroxidase(GSH-Px)were measured.The protein levels of nuclear factor-κB(NF-κB)p65,p-p65,IκB and pIκB in lung tissues were detected by Western blot.RESULTS:The lung tissue showed typical inflammatory changes and obvious damage,and the lung W/D ratio was significantly increased in model group(P<0.01).The serum levels of IL-1β,IL-18,TNF-α,IL-6,MDA and MPO,and the NF-κB protein expression in lung tissues were significantly increased(P<0.01),while the serum levels of CAT,GSH and GSH-Px were significantly decreased in model group(P<0.01).Pretreatment with PLD alleviated pathological damage of lung tissues,reduced the lung W/D weight ratio(P<0.01),and decreased the serum levels of IL-1β,IL-18,TNF-α,IL-6,MDA and MPO as well as the NF-κB expression in lung tissues.It also increased serum CAT,GSH and GSH-Px activity significantly(P<0.05 or P<0.01).CONCLUSION:Pretreatment with PLD alleviates the damage of lung tissues in LPS-induced ALI rats by inhibiting NF-κB pathway.
作者
裴彩霞
王振兴
汪晓敏
吴永灿
黄德美
杨琪
王飞
PEI Cai-xia;WANG Zhen-xing;WANG Xiao-min;WU Yong-can;Huang De-mei;Yang Qi;WANG Fei(Hospital of Chengdu University of Traditional Chinese Medicine,Chengdu 610075,China;Sichuan College of Tradi-tional Chinese Medicine,Mianyang 621000,China)
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2022年第4期672-679,共8页
Chinese Journal of Pathophysiology
基金
四川省学术和技术带头人培养支持经费(No.008075005)
四川省科技厅重点研发计划(No.2020YFS0312)。
关键词
急性肺损伤
脂多糖
桔梗皂苷D
核因子ΚB
Acute lung injury
Lipopolysaccharide
Platycodin D
Nuclear factor-κB
