虎杖苷通过SIRT3减轻脂多糖诱导的肺泡上皮细胞氧化应激  

Polydatin alleviates lipopolysaccharide-induced oxidative stress in the alveolar epithelial cells via SIRT3

作　　者：段智[1] 艾晨牧 王香 雷小保[1] Duan Zhi;Ai Chenmu;Wang Xiang;Lei Xiaobao(Department of Critical Care Medicine,Chenzhou No.1 People’s Hospital,Chenzhou 423000,China)

机构地区：[1]郴州市第一人民医院重症医学科,423000

出　　处：《国际医药卫生导报》2020年第9期1186-1188,共3页International Medicine and Health Guidance News

基　　金：湖南省自然科学基金(2018JJ3015,2018JJ6004);郴州市第一人民医院课题(N2019-057)。

摘　　要：目的探讨虎杖苷对脂多糖(LPS)诱导的肺泡上皮细胞氧化应激的影响及其可能机制。方法A549细胞随机分为5组:对照组细胞不接受任何刺激;溶剂组细胞只接受DMSO处理;模型组细胞接受5μg/ml LPS刺激6 h;治疗组细胞接受5μg/ml LPS及50μmol/L虎杖苷刺激6 h;抑制剂组细胞接受5μg/ml LPS、50μmol/L虎杖苷及50μmol/L 3-TYP刺激6 h。采用试剂盒分别检测细胞SIRT3活性、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力、总抗氧化能力(T-AOC)、细胞毒性及活力。结果与对照组比较,模型组MDA含量及细胞毒性分别显著增加为(5.35±0.53)nmol/(mg·pr)及(264±25.9)U/L,SIRT3活性、T-AOC、SOD活性及细胞活力显著下降为(69±6.5)%、(25.8±3.5)μmol/(mg·pr)、(0.49±0.19)U/(mg·pr)及(74±5.7)%(均P<0.05)。与模型组比较,治疗组MDA含量及细胞毒性分别显著下降为(3.51±0.39)nmol/(mg·pr)及(171±19.5)U/L,SIRT3活性、T-AOC、SOD活性及细胞活力显著增加为(87±6.0)%、(0.91±0.21)μmol/(mg·pr)、(18.5±6.4)U/(mg·pr)及(89±5.5)%(均P<0.05)。与治疗组比较,抑制剂组MDA含量及细胞毒性分别显著增加为(5.27±0.5)nmol/(mg·pr)及(244±24.6)U/L,SIRT3活性、T-AOC、SOD活性及细胞活力显著下降为(74±5.4)%、(0.53±0.18)μmol/(mg·pr)、(18.5±6.4)U/(mg·pr)及(77±5.9)%(均P<0.05)。结论虎杖苷显著减轻LPS诱导的肺泡上皮细胞氧化应激,其机制可能与激活SIRT3有关。Objective To investigate the effects and potential mechanism of polydatin on the lipopolysaccharide-induced oxidative stress of the alveolar epithelial cells.Methods A549 cells were randomly divided into five groups:the cells in the control group received none treatment;the cells in the vehicle group received the treatment with DMSO for 6 hours;the cells in the model group received the treatment with LPS(5μg/L)for 6 hours;the cells in the treatment group received the treatment with LPS(5μg/L)and polydatin(50μmol/L)for 6 hours;the cells in the inhibitor group received the treatment with LPS(5μg/L),polydatin(50μmol/L),and 3-TYP(50μmol/L)for 6 hours.The SIRT3 activity,malondialdehyde(MDA)content,superoxide dismutase(SOD)activity,total antioxidant capacity(T-AOC),cytotoxicity,and cell viability were measured by the commercial assay kits.Results Compared with the control group,the MDA content and cytotoxicity in the model group respectively increased to(5.35±0.53)nmol/(mg pr)and(264±25.9)U/L;the SIRT3 activity,T-AOC,SOD activity,and cell viability respectively decreased to(69±6.5)%,(25.8±3.5)μmol/(mg pr),(0.49±0.19)U/(mg pr),(74±5.7)%(all P<0.05).Compared with the model group,the MDA content and cytotoxicity in the treatment group respectively decreased to(3.51±0.39)nmol/(mg pr)and(171±19.5)U/L;the SIRT3 activity,T-AOC,SOD activity,and cell viability respectively increased to(87±6.0)%,(0.91±0.21)μmol/(mg pr),(18.5±6.4)U/(mg pr),and(89±5.5)%(all P<0.05).Compared with the treatment group,the MDA content and cytotoxicity in the inhibitor group respectively increased to(5.27±0.5)nmol/(mg pr)and(244±24.6)U/L;the SIRT3 activity,T-AOC,SOD activity,and cell viability respectively decreased to(74±5.4)%,(0.53±0.18)μmol/(mg pr),(18.5±6.4)U/(mg pr),and(77±5.9)%(all P<0.05).Conclusion Polydatin significantly alleviates LPS-induced oxidative stress of the alveolar epithelial cells,the mechanism of which may be related to the activation of SIRT3.

关 键 词：虎杖苷 氧化应激 肺泡上皮细胞 脂多糖 

分 类 号：R285.5[医药卫生—中药学]