中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
11期
2764-2766
,共3页
刘红梅%马利军%秦涛%张罗献
劉紅梅%馬利軍%秦濤%張囉獻
류홍매%마리군%진도%장라헌
间充质干细胞%香烟烟雾提取物%肿瘤坏死因子-α-刺激基因-6
間充質榦細胞%香煙煙霧提取物%腫瘤壞死因子-α-刺激基因-6
간충질간세포%향연연무제취물%종류배사인자-α-자격기인-6
Mesenchymal stem cells%Cigarette smoke extract%Tumor necrosis factor-α-stimulating gene 6
目的 观察骨髓间充质干细胞(MSCs)对香烟烟雾提取物(CSE)诱导的巨噬细胞炎性反应的抗炎机制.方法 A:RAW264.7对照组,B:RAW264.7+CSE组,C: RAW264.7+CSE+MSCs组,D:RAW264.7+CSE+TSG-6小干扰RNA (siRNA) MSCs组,E:RAW264.7+CSE+ siRNA MSCs组.测定MSCs分泌肿瘤坏死因子-α-刺激基因-6(TSG-6)、细胞因子、M2巨噬细胞标志CD206、核因子-κB(NF-κB) p65水平.结果 肿瘤坏死因子-α(TNF-α)刺激MSCs分泌高水平TSG-6.与A组比较,B组NF-κB p65增高[(0.442±0.080)比(0.127±0.020),P<0.01],促炎因子增高.与B组比较,C组CD206增高[(0.242 ±0.010)比(0.096±0.002),P<0.01],NF-κB p65减少[(0.265±0.030)比(0.442±0.080),P<0.01],促炎因子减少.结论 MSCs分泌TSG-6促使巨噬细胞由M1型向M2型转化,抑制CSE诱导的NF-κB信号通路和炎性反应.
目的 觀察骨髓間充質榦細胞(MSCs)對香煙煙霧提取物(CSE)誘導的巨噬細胞炎性反應的抗炎機製.方法 A:RAW264.7對照組,B:RAW264.7+CSE組,C: RAW264.7+CSE+MSCs組,D:RAW264.7+CSE+TSG-6小榦擾RNA (siRNA) MSCs組,E:RAW264.7+CSE+ siRNA MSCs組.測定MSCs分泌腫瘤壞死因子-α-刺激基因-6(TSG-6)、細胞因子、M2巨噬細胞標誌CD206、覈因子-κB(NF-κB) p65水平.結果 腫瘤壞死因子-α(TNF-α)刺激MSCs分泌高水平TSG-6.與A組比較,B組NF-κB p65增高[(0.442±0.080)比(0.127±0.020),P<0.01],促炎因子增高.與B組比較,C組CD206增高[(0.242 ±0.010)比(0.096±0.002),P<0.01],NF-κB p65減少[(0.265±0.030)比(0.442±0.080),P<0.01],促炎因子減少.結論 MSCs分泌TSG-6促使巨噬細胞由M1型嚮M2型轉化,抑製CSE誘導的NF-κB信號通路和炎性反應.
목적 관찰골수간충질간세포(MSCs)대향연연무제취물(CSE)유도적거서세포염성반응적항염궤제.방법 A:RAW264.7대조조,B:RAW264.7+CSE조,C: RAW264.7+CSE+MSCs조,D:RAW264.7+CSE+TSG-6소간우RNA (siRNA) MSCs조,E:RAW264.7+CSE+ siRNA MSCs조.측정MSCs분비종류배사인자-α-자격기인-6(TSG-6)、세포인자、M2거서세포표지CD206、핵인자-κB(NF-κB) p65수평.결과 종류배사인자-α(TNF-α)자격MSCs분비고수평TSG-6.여A조비교,B조NF-κB p65증고[(0.442±0.080)비(0.127±0.020),P<0.01],촉염인자증고.여B조비교,C조CD206증고[(0.242 ±0.010)비(0.096±0.002),P<0.01],NF-κB p65감소[(0.265±0.030)비(0.442±0.080),P<0.01],촉염인자감소.결론 MSCs분비TSG-6촉사거서세포유M1형향M2형전화,억제CSE유도적NF-κB신호통로화염성반응.
Objective To study the anti-inflammatory mechanism of bone marrow mesenchymal stem cells (MSCs) in inflammatory response of macrophage induced by cigarette smoke extract (CSE).Methods Five groups were established in the experiment: A, RAW264.7 group;B, RAW264.7 + CSE group;C, RAW264.7 + CSE + MSCs group;D, RAW264.7 + CSE + TSG small interfering RNA (siRNA) MSCs group;E, RAW264.7 + CSE + siRNA MSCs group.The expression of tumor necrosis factor-α-stimulating gene 6 (TSG-6) induced by MSCs, cytokine, nuclear factor-κB (NF-κB) p65 and CD206 was detected.Results MSCs stimulated by tumor necrosis factor-α (TNF-α) could secrete high levels of TSG-6.As compared with group A, the expression of NF-κB p65 in macrophage nucleus was significantly increased [(0.442 ±0.080) vs.(0.127 ±0.020), P <0.01] and the proinflammatory cytokine was significantly increased in group B.As compared with group B, M2 macrophages detected by CD206 expression were significantly increased in group C [(0.242 ±0.010) vs.(0.096 ±0.002), P < 0.01], the expression of NF-κB p65 was decreased [(0.265 ± 0.030) vs.(0.442 ± 0.080), P < 0.01], and the expression of proinflammatory cytokines was decreased in group C.Conclusion MSCs can attenuate the inflammatory cascade and inhibit the action of NF-κB induced by CSE through inducing macrophages conversion from M1 type to M2 type by secreting TSG-6.