国际流行病学传染病学杂志
國際流行病學傳染病學雜誌
국제류행병학전염병학잡지
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY AND INFECTIOUS DISEASE
2010年
4期
244-247
,共4页
舒旷怡%李方去%杨锦红%杨爱平%陶洪群%陈慧%李向阳
舒曠怡%李方去%楊錦紅%楊愛平%陶洪群%陳慧%李嚮暘
서광이%리방거%양금홍%양애평%도홍군%진혜%리향양
脂多糖类%脂蛋白%肿瘤坏死因子-α
脂多糖類%脂蛋白%腫瘤壞死因子-α
지다당류%지단백%종류배사인자-α
Lipopolysaccharides%Lipoproteins%Tumor necrosis factor-α
目的 研究血清脂蛋白对脂多糖的影响机制,并对不同种类脂蛋白:高密度脂蛋白(HDL)、低密度脂蛋白(LDL)和极低密度脂蛋白(VLDL),抑制脂多糖的能力进行比较,为研究脂蛋白在治疗败血症中的应用提供理论基础.方法 通过检测经佛波醇酯刺激分化的THP-1细胞分泌的TNF-α间接反映脂蛋白对脂多糖的抑制作用.将不同浓度脂多糖与THP-1细胞在血清基质中混合孵育4 h,并与3种脂蛋白-脂多糖混合液与THP-1细胞混合孵育后TNF-α的分泌量进行对比,计算脂蛋白对脂多糖的抑制情况.结果 HDL、LDL和VLDL单独不能诱导分化的THP-1细胞分泌TNF-α(P＞0.05).当10 ng/mL脂多糖与0.05 mg/m以上浓度的脂蛋白(HDL、LDL和VLDL)混合时,TNF-α分泌量明显降低.当脂多糖浓度为100 ng/mL时,0.1 mg/mL的脂蛋白(HDL、LDL和VLDL)对其抑制效果较低,分别为(20.7±11.1)%、(8.9±2.8)%、(4.3±1.6)%;在脂多糖浓度为10 ng/mL抑制效果明显增强,抑制率分别为(69.3±3.7)%、(42.9±5.7)%、(42.7±4.5)%.HDL对各浓度脂多糖的抑制效果均强于LDL和VLDL(P＜0.05).结论 脂蛋白在血清中能抑制脂多糖活化巨噬细胞分泌细胞因子,但抑制效果在脂多糖浓度高时相比浓度低时差.HDL对脂多糖活化巨噬细胞的抑制作用比LDL和VLDL强.
目的 研究血清脂蛋白對脂多糖的影響機製,併對不同種類脂蛋白:高密度脂蛋白(HDL)、低密度脂蛋白(LDL)和極低密度脂蛋白(VLDL),抑製脂多糖的能力進行比較,為研究脂蛋白在治療敗血癥中的應用提供理論基礎.方法 通過檢測經彿波醇酯刺激分化的THP-1細胞分泌的TNF-α間接反映脂蛋白對脂多糖的抑製作用.將不同濃度脂多糖與THP-1細胞在血清基質中混閤孵育4 h,併與3種脂蛋白-脂多糖混閤液與THP-1細胞混閤孵育後TNF-α的分泌量進行對比,計算脂蛋白對脂多糖的抑製情況.結果 HDL、LDL和VLDL單獨不能誘導分化的THP-1細胞分泌TNF-α(P＞0.05).噹10 ng/mL脂多糖與0.05 mg/m以上濃度的脂蛋白(HDL、LDL和VLDL)混閤時,TNF-α分泌量明顯降低.噹脂多糖濃度為100 ng/mL時,0.1 mg/mL的脂蛋白(HDL、LDL和VLDL)對其抑製效果較低,分彆為(20.7±11.1)%、(8.9±2.8)%、(4.3±1.6)%;在脂多糖濃度為10 ng/mL抑製效果明顯增彊,抑製率分彆為(69.3±3.7)%、(42.9±5.7)%、(42.7±4.5)%.HDL對各濃度脂多糖的抑製效果均彊于LDL和VLDL(P＜0.05).結論 脂蛋白在血清中能抑製脂多糖活化巨噬細胞分泌細胞因子,但抑製效果在脂多糖濃度高時相比濃度低時差.HDL對脂多糖活化巨噬細胞的抑製作用比LDL和VLDL彊.
목적 연구혈청지단백대지다당적영향궤제,병대불동충류지단백:고밀도지단백(HDL)、저밀도지단백(LDL)화겁저밀도지단백(VLDL),억제지다당적능력진행비교,위연구지단백재치료패혈증중적응용제공이론기출.방법 통과검측경불파순지자격분화적THP-1세포분비적TNF-α간접반영지단백대지다당적억제작용.장불동농도지다당여THP-1세포재혈청기질중혼합부육4 h,병여3충지단백-지다당혼합액여THP-1세포혼합부육후TNF-α적분비량진행대비,계산지단백대지다당적억제정황.결과 HDL、LDL화VLDL단독불능유도분화적THP-1세포분비TNF-α(P＞0.05).당10 ng/mL지다당여0.05 mg/m이상농도적지단백(HDL、LDL화VLDL)혼합시,TNF-α분비량명현강저.당지다당농도위100 ng/mL시,0.1 mg/mL적지단백(HDL、LDL화VLDL)대기억제효과교저,분별위(20.7±11.1)%、(8.9±2.8)%、(4.3±1.6)%;재지다당농도위10 ng/mL억제효과명현증강,억제솔분별위(69.3±3.7)%、(42.9±5.7)%、(42.7±4.5)%.HDL대각농도지다당적억제효과균강우LDL화VLDL(P＜0.05).결론 지단백재혈청중능억제지다당활화거서세포분비세포인자,단억제효과재지다당농도고시상비농도저시차.HDL대지다당활화거서세포적억제작용비LDL화VLDL강.
Objective To investigate the affect mechanism of serum lipoproteins(HDL, LDL, VLDL) on LPS,and compare the regulation ability in LPS-activated of them, to provide theoretical basis for the application of lipoprotein in treatment of sepsis. Methods TNF-α secreted from PMA-differentiated THP-1 cell were detected to reflect the inhibitory action of lipoprotein on LPS indirectly. THP-1 cell were incubated with LPS for 4 houris, TNF-α levels were detected and then compared with the levels in which THP-1 cell incubated with lipoprotein-LPS mixture. Futhermore, the inhibitory action from lipoprotein to LPS was estimated. Results HDL, LDL and VLDL did not induce differentiated THP-1 cells to secrete TNF-α( P ＞ 0.05). When lipoprotein was above 0.05 mg/mL and mixed with 10 ng/mL LPS,TNF-α decreased obviously. The inhibition action of 0. 1 mg/mL lipoprotein (HDL, LDL, VLDL) on LPS was low when LPS was 100 ng/mL, and the rates were (20.7± 11.1)%, (8.85+2.75)%, (4.3± 1.6)% respectively; the inhibitory effect was significantly increased when LPS was 10 ng/mL, and the rates were (69.3±3.7)%, (42.9±5.7)%,(42.7±4.5)% respectively. HDL had stronger inhibitory effect than LDL and VLDL(P ＜ 0.05). ConclusionsLipoprotein in serum can inhibit LPS-activated macrophage cells to secrete cytolines, but the inhibition of lipoprotein is more obvious in high concentration of LPS than low concentration. HDL has a stronger inhibitory effect on LPS activation than LDL and VLDL.
