肠外与肠内营养
腸外與腸內營養
장외여장내영양
PARENTERAL & ENTERAL NUTRITION
2010年
1期
29-31
,共3页
王立明%王新颖%潘莉雅%张峰%黎介寿
王立明%王新穎%潘莉雅%張峰%黎介壽
왕립명%왕신영%반리아%장봉%려개수
谷氨酰胺%内毒素%细胞因子%P38MAPK
穀氨酰胺%內毒素%細胞因子%P38MAPK
곡안선알%내독소%세포인자%P38MAPK
Glutamine%Lipopolysaccharide%Cytokine%P38MAPK
目的:探讨谷氨酰胺(Gln)抑制人外周血单个核细胞(PBMC)细胞因子过度表达的分子机制.方法: 用Ficoll密度梯度离心法提取健康志愿者新鲜外周血单个核细胞,在培养液中加入Gln、P38MAPK通路阻滞剂(SB203580)和HSP70阻断剂(Quercetin),用内毒素刺激4 h后,留取细胞和上清液,ELISA法测定内毒素刺激下单个核细胞肿瘤坏死因子(TNF-α)和IL-10的表达,Western blot方法检测细胞内磷酸化P38的表达情况. 结果: Gln能明显增加HSP70的表达,同时TNF-α和IL-10表达受抑;使用Quercetin和SB203580后,磷酸化P38减少的同时TNF-α和IL-10也减少了. 结论: Gln下调LPS刺激下PBMC细胞因子的过度表达依赖于P38MAPK信号蛋白的抑制.
目的:探討穀氨酰胺(Gln)抑製人外週血單箇覈細胞(PBMC)細胞因子過度錶達的分子機製.方法: 用Ficoll密度梯度離心法提取健康誌願者新鮮外週血單箇覈細胞,在培養液中加入Gln、P38MAPK通路阻滯劑(SB203580)和HSP70阻斷劑(Quercetin),用內毒素刺激4 h後,留取細胞和上清液,ELISA法測定內毒素刺激下單箇覈細胞腫瘤壞死因子(TNF-α)和IL-10的錶達,Western blot方法檢測細胞內燐痠化P38的錶達情況. 結果: Gln能明顯增加HSP70的錶達,同時TNF-α和IL-10錶達受抑;使用Quercetin和SB203580後,燐痠化P38減少的同時TNF-α和IL-10也減少瞭. 結論: Gln下調LPS刺激下PBMC細胞因子的過度錶達依賴于P38MAPK信號蛋白的抑製.
목적:탐토곡안선알(Gln)억제인외주혈단개핵세포(PBMC)세포인자과도표체적분자궤제.방법: 용Ficoll밀도제도리심법제취건강지원자신선외주혈단개핵세포,재배양액중가입Gln、P38MAPK통로조체제(SB203580)화HSP70조단제(Quercetin),용내독소자격4 h후,류취세포화상청액,ELISA법측정내독소자격하단개핵세포종류배사인자(TNF-α)화IL-10적표체,Western blot방법검측세포내린산화P38적표체정황. 결과: Gln능명현증가HSP70적표체,동시TNF-α화IL-10표체수억;사용Quercetin화SB203580후,린산화P38감소적동시TNF-α화IL-10야감소료. 결론: Gln하조LPS자격하PBMC세포인자적과도표체의뢰우P38MAPK신호단백적억제.
Objective: To investigate the mechanism that glutamine downregulates the cytokine expression in lipopolysaccharide-stimulated human peripheral blood mononuclear cells.Methods:PMBC were extracted from healthy volunteer by density gradient centrifugation,and stimulated by lipopolysaccharide.The release of TNF-α and IL-10 was analyzed via enzyme-linked immunosorbent assay and p-P38 via western blot. Results:Gln led to an increase in HSP70 expression,and decreased TNF-α、IL-10 release at 4 h after LPS stimulation.The expressions level of TNF-α、IL-10 and P-P38 were decreased after using SB203580.Conclusion:These results indicate that the effect of Gln could attenuate cytokine release in PBMC and might may be related to the inhibition of P38 MAPK.