中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2015年
6期
664-666
,共3页
李俊%李婷婷%张鹏%刘天骄%黄承敏%高海青%郭媛
李俊%李婷婷%張鵬%劉天驕%黃承敏%高海青%郭媛
리준%리정정%장붕%류천교%황승민%고해청%곽원
肿瘤坏死因子%动脉粥样硬化
腫瘤壞死因子%動脈粥樣硬化
종류배사인자%동맥죽양경화
Tumor necrosis factor%Atherosclerosis
目的 探究肿瘤坏死因子相关蛋白9(CTRP9)对氧化型低密度脂蛋白(ox-LDL)诱导RAW 264.7小鼠巨噬细胞抗炎作用和机制. 方法 选择RAW264.7小鼠巨噬细胞系,分为对照组(对照组)、oxLDL组、gCTRP9+ oxLDL组.采用油红O染色鉴定泡沫细胞,免疫印迹分析检测肿瘤坏死因子(TNF)-α、单核细胞趋化蛋白(MCP-1)及胞浆、细胞核核转录因子κB (NF-κB) p65蛋白表达水平. 结果 与对照组比较,ox-LDL组巨噬泡沫细胞中MCP-1蛋白和TNF-α蛋白表达上调(P<0.05),与ox-LDL组比较,gCTRP9+ oxLDL组TNF-α和MCP-1的蛋白表达降低(P<0.05).oxLDL组与对照组比较,NF-κB表达增加(P<0.05);与ox-LDL组比较,gCTRP9组2h和8hNFκB P65表达下降,1.03±0.06比0.17±0.10和0.31±0.03(均P<0.05). 结论 oxLDL可诱导巨噬细胞表达TNF-α和MCP-1,gCTRP9可减少oxLDL的促炎作用,NF-κB信号转导通路可能参与了上述抗炎作用机制,提示gCTRP9可能具有抗炎,抗动脉粥样硬化的保护性作用.
目的 探究腫瘤壞死因子相關蛋白9(CTRP9)對氧化型低密度脂蛋白(ox-LDL)誘導RAW 264.7小鼠巨噬細胞抗炎作用和機製. 方法 選擇RAW264.7小鼠巨噬細胞繫,分為對照組(對照組)、oxLDL組、gCTRP9+ oxLDL組.採用油紅O染色鑒定泡沫細胞,免疫印跡分析檢測腫瘤壞死因子(TNF)-α、單覈細胞趨化蛋白(MCP-1)及胞漿、細胞覈覈轉錄因子κB (NF-κB) p65蛋白錶達水平. 結果 與對照組比較,ox-LDL組巨噬泡沫細胞中MCP-1蛋白和TNF-α蛋白錶達上調(P<0.05),與ox-LDL組比較,gCTRP9+ oxLDL組TNF-α和MCP-1的蛋白錶達降低(P<0.05).oxLDL組與對照組比較,NF-κB錶達增加(P<0.05);與ox-LDL組比較,gCTRP9組2h和8hNFκB P65錶達下降,1.03±0.06比0.17±0.10和0.31±0.03(均P<0.05). 結論 oxLDL可誘導巨噬細胞錶達TNF-α和MCP-1,gCTRP9可減少oxLDL的促炎作用,NF-κB信號轉導通路可能參與瞭上述抗炎作用機製,提示gCTRP9可能具有抗炎,抗動脈粥樣硬化的保護性作用.
목적 탐구종류배사인자상관단백9(CTRP9)대양화형저밀도지단백(ox-LDL)유도RAW 264.7소서거서세포항염작용화궤제. 방법 선택RAW264.7소서거서세포계,분위대조조(대조조)、oxLDL조、gCTRP9+ oxLDL조.채용유홍O염색감정포말세포,면역인적분석검측종류배사인자(TNF)-α、단핵세포추화단백(MCP-1)급포장、세포핵핵전록인자κB (NF-κB) p65단백표체수평. 결과 여대조조비교,ox-LDL조거서포말세포중MCP-1단백화TNF-α단백표체상조(P<0.05),여ox-LDL조비교,gCTRP9+ oxLDL조TNF-α화MCP-1적단백표체강저(P<0.05).oxLDL조여대조조비교,NF-κB표체증가(P<0.05);여ox-LDL조비교,gCTRP9조2h화8hNFκB P65표체하강,1.03±0.06비0.17±0.10화0.31±0.03(균P<0.05). 결론 oxLDL가유도거서세포표체TNF-α화MCP-1,gCTRP9가감소oxLDL적촉염작용,NF-κB신호전도통로가능삼여료상술항염작용궤제,제시gCTRP9가능구유항염,항동맥죽양경화적보호성작용.
Objective To investigate the anti-inflammatory effect of C1q/ tumor necrosis factor (TNF)-related protein 9 (CTRP9) in RAW264.7 mouse macrophage cells treated with oxidized low density lipoprotein (oxLDL),and to explore its mechanism.Methods RAW264.7 mouse macrophage cells were divided into three groups:the control group,the oxLDL group (treated with oxLDl) and the gCTRP9-oxLDL group (pretreated with recombinant globular domain of CTRP9 and stimulated by oxLDL).Foam cells were detected by oil red O staining.Western blot was used to detect the expressions of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein 1 (MCP-1).In addition,the expression levels of NF-κB p65 in cytoplasm and nucleus proteins extraction were both determined.Results The relative levels of MCP-1 and NF-κB were increased in the oxLDL group as compared with the control group (1.66±0.09 vs.1.03±0.10,0.52±0.11 vs.1.03±0.06,both P<0.05).The expression levels of TNF-α and MCP-1 were decreased in gCTRP9+oxLDL group as compared with the oxLDL group (both P<0.05).The expression level of NF κB p65 in nucleus 2 and 8 h after treatment was lower in the gCTRP9+oxLDL group than in the oxLDL group (1.03±0.06 vs.0.17±0.10,0.31±0.03,both P<0.05).Conclusions oxLDL may induce the expressions of inflammatory cytokines of TNF α and MCP-1 in macrophage ceils.gCTRP9 pretreatment could reduce the oxLDL-induced pro inflammatory effect and nuclear factor κB translocation may be involved in this process,which suggests that gCTRP9 may play a protective role in anti inflammatory and anti-atherosclerosis.