医学研究杂志
醫學研究雜誌
의학연구잡지
Journal of Medical Research
2015年
10期
110-113
,共4页
叶婷婷%王光宇%李丽%马建%魏盟
葉婷婷%王光宇%李麗%馬建%魏盟
협정정%왕광우%리려%마건%위맹
白藜芦醇%脂多糖%ERK1/2%H9%c2细胞
白藜蘆醇%脂多糖%ERK1/2%H9%c2細胞
백려호순%지다당%ERK1/2%H9%c2세포
Resveratrol%Lipopolysaccharide%H9c2 cardiomyocytes%p-ERK1/2
目的 探讨白藜芦醇(resveratrol,RSV)是否通过下调p-ERK1/2 发挥对脂多糖(lipopolysaccharide,LPS)诱导的H9c细胞氧化损伤的保护作用及机制. 方法 将H9c2细胞分为实验( Con)组,脂多糖( LPS)组,脂多糖+白藜芦醇5μmol/L (L+R5)组,脂多糖+白藜芦醇10μmol/L(L+R10)组,脂多糖+白藜芦醇20μmol/L(L+R20)组,脂多糖+白藜芦醇50μmol/L (L+R50)组. 其中对照组不做任何处理,L+R5组、L+R10组、L+R20组、L+R50组分别用5、10、20、50μmol/L的白藜芦醇预先处理24h,然后将LPS组、L+R5组、L+R10组、L+R20组、L+R50组和10μg/ml的脂多糖共同孵育20min和12h. MTT比色法检测H9c2细胞活力,Western blot法检测p-ERK1/2,ERK1/2蛋白表达. 结果 LPS降低H9c2细胞活力,诱导细胞凋亡.RSV上调p-ERK1/2蛋白表达,成剂量依赖性. RSV预处理能明显降低LPS对H9c2细胞的损伤. 结论 白藜芦醇可能通过下调p-ERK1/2 来减轻LPS引起的H9c2 细胞损伤,发挥其保护作用.
目的 探討白藜蘆醇(resveratrol,RSV)是否通過下調p-ERK1/2 髮揮對脂多糖(lipopolysaccharide,LPS)誘導的H9c細胞氧化損傷的保護作用及機製. 方法 將H9c2細胞分為實驗( Con)組,脂多糖( LPS)組,脂多糖+白藜蘆醇5μmol/L (L+R5)組,脂多糖+白藜蘆醇10μmol/L(L+R10)組,脂多糖+白藜蘆醇20μmol/L(L+R20)組,脂多糖+白藜蘆醇50μmol/L (L+R50)組. 其中對照組不做任何處理,L+R5組、L+R10組、L+R20組、L+R50組分彆用5、10、20、50μmol/L的白藜蘆醇預先處理24h,然後將LPS組、L+R5組、L+R10組、L+R20組、L+R50組和10μg/ml的脂多糖共同孵育20min和12h. MTT比色法檢測H9c2細胞活力,Western blot法檢測p-ERK1/2,ERK1/2蛋白錶達. 結果 LPS降低H9c2細胞活力,誘導細胞凋亡.RSV上調p-ERK1/2蛋白錶達,成劑量依賴性. RSV預處理能明顯降低LPS對H9c2細胞的損傷. 結論 白藜蘆醇可能通過下調p-ERK1/2 來減輕LPS引起的H9c2 細胞損傷,髮揮其保護作用.
목적 탐토백려호순(resveratrol,RSV)시부통과하조p-ERK1/2 발휘대지다당(lipopolysaccharide,LPS)유도적H9c세포양화손상적보호작용급궤제. 방법 장H9c2세포분위실험( Con)조,지다당( LPS)조,지다당+백려호순5μmol/L (L+R5)조,지다당+백려호순10μmol/L(L+R10)조,지다당+백려호순20μmol/L(L+R20)조,지다당+백려호순50μmol/L (L+R50)조. 기중대조조불주임하처리,L+R5조、L+R10조、L+R20조、L+R50조분별용5、10、20、50μmol/L적백려호순예선처리24h,연후장LPS조、L+R5조、L+R10조、L+R20조、L+R50조화10μg/ml적지다당공동부육20min화12h. MTT비색법검측H9c2세포활력,Western blot법검측p-ERK1/2,ERK1/2단백표체. 결과 LPS강저H9c2세포활력,유도세포조망.RSV상조p-ERK1/2단백표체,성제량의뢰성. RSV예처리능명현강저LPS대H9c2세포적손상. 결론 백려호순가능통과하조p-ERK1/2 래감경LPS인기적H9c2 세포손상,발휘기보호작용.
Objective To investigate whether resveratrol ( RSV) protects H9c2 cells against lipopolysaccharide ( LPS) induced oxi-dative injury partly through ERK1/2 signaling pathway.Methods H9c2 cells were divided into six groups:control, LPS (10μg/ml li-popolysaccharide),L+R5(10μg/ml lipopolysaccharide +5 μmol/L resveratrol),L+R10(10μg/ml lipopolysaccharide +10μmol/L res-veratrol),L+R20(10μg/ml lipopolysaccharide +20 μmol/L resveratrol),L +R50(10μg/ml lipopolysaccharide +50μmol/L resvera-trol).H9c2 cells from group L+R5 ,L+R10,L+R20,L+R50 were pretreated with resveratrol .Then, cells from group LPS ,L+R5,L+R10,L+R20,L+R50 were incubated with LPS for 20 min and 12 hours.MTT were used to detect cell proliferation .The protein level of ERK1/2, and phosphorylation of ERK 1/2 was measured by Western blot respectively .Results Compared with control , LPS signifi-cantly reduced cell proliferation (P<0.05), increased(P<0.01)cell death, and up-regulated the level of phosphorylation of ERK 1/2(P<0.01).Pretreatment of resveratrol attenuated the inhibition of LPS on cell viability and down -regulated the level of phosphoryla-tion of ERK1/2.Conclusion Resveratrol may exert its cytoprotection effects on LPS -induced H9c2 cells via down regulating the activa-tion of p-ERK1/2