The effect of Propofol on the activation of p38 MAPK/NF-κB signal pathway in human umbilical vein endothelial cells induced by lipopolysaccharide
WANG Xin1,2;LEI Xiao-wen1;CHEN Dan1;LIU Bin2
1.Department of Anesthesia,Guizhou Provincial People′s Hospital,Guiyang 550002,China;2.Department of Anesthesia,West China Hospital of Sichuan University,Chengdu 610041,China
Abstract:bjective To study the influence of Propofol on the activity of p38,MAPK/NF-κ B signal pathway in human umbilical vein endothelial cells(HUBECs)induced by lipopolysaccharide (LPS).Methods HUBECs cultured in vitro were randomly divided into the 4 groups:control group(group C)was given Intralipid 20 mg/L,LPS group(L group)was given LPS 10 mg/L,Propofol group (P group)was given Propofol 20 mg/L,Propofol+LPS group (PL group)was given Propofol 20 mg/L and LPS 10 mg/L.The change in the content of p38 MAPK,p-p38 MAPK and NF-κB were detected at five time points of 1,2,3,6,and 12 h.Results When administered 1 h,the gray value of p-p38 MAPK and NF-κB in group L was 10.32±0.73,60.32±5.73 respectively,which increased significantly compared with group C(P<0.05).When administered 2 h,the gray value of p-p38 MAPK and NF-κB in group L was 9.23 ±0.53,69.23±5.53,which increased significantly compared with group C (P<0.05),and the gray value of PL group was 6.32±0.35,which was significantly lower than that of group L.Administration of 3 h,p-p38 MAPK,NF-κB gray value in group L was 11.13±0.23,71.13±5.23 respectively,which increased significantly compared with group C(P<0.05).p-p38 MAPK,NF-κB gray value was 8.95±0.21,56.95±5.21 respectively in group PL,which decreased significantly compared with group L(P<0.05).Administration of 6 h,p-p38 MAPK,NF-κB gray value was 12.16±0.20,73.16±4.20 respectively in group L,which increased significantly compared with group C (P<0.05).p-p38 MAPK,NF-κB gray value was 9.65±0.32,58.65±4.32 respectively in group PL,which decreased significantly compared with the L group (P<0.05).Administration of 12 h,p-p38 MAPK,NF-κB gray value was 18.19±0.31,91.19±6.31 respectively,which increased significantly compared with group C (P<0.05).p-p38 MAPK,NF-κB gray value in group PL was 12.65±0.12,63.36±5.12 respectively,which decreased significantly compared with group L(P<0.05).Conclusion LPS stimulating HUBECs can increase the expression of p-p38 MAPK and NF-κB,and inhibit this increase after Propofol injection may be one of the mechanisms of Propofol anti-inflammation.
汪鑫; 雷晓文 ;陈丹;刘斌. 丙泊酚对脂多糖诱导的人脐静脉内皮细胞p38 MAPK/NF-κB信号通路活性的影响[J]. 中国当代医药, 2018, 25(9): 4-6转11.
WANG Xin;LEI Xiao-wen;CHEN Dan;LIU Bin. The effect of Propofol on the activation of p38 MAPK/NF-κB signal pathway in human umbilical vein endothelial cells induced by lipopolysaccharide. 中国当代医药, 2018, 25(9): 4-6转11.
FrohlicD,TraboldB,RotheeG,etal.Inhibitionoftheneutrophil oxidative response by propofol:preserved in vivo function despite in vitro inhibition[J].Eur J Anaesthesiol,2006,23(11):948-953.
[2]
O′Donnell NG,McSharry CP,Wilkinson PC,et al.Comparison of the inhibitory effect of propofol,thiopentone and midazolam on neutrophil polarization in vitro in the presence or absence of human serum albumin[J].Br J Anaesth,1992,69(1):70-74.
[3]
Liu MC,Tsai PS,Yang CH,et al.Propofol significantly attenuates iNOS,CAT-2,and CAT-2B transcription in lipopolys a ccharide-stimulated murine macrophages[J].Acta Anaesthesiol Taiwan,2006,44(2):73-81.
[4]
Corcoran TB,O′Shea A,Engel A,et al.The influence of propofol on P-selectin expression and nitric oxide production in re-oxygenated human umbilical vein endothelial cells[J].Acta Anaesthesiol Scand,2006,50(3):348-354.
[5]
Sun HY,Xue FS,Xu YC,et al.Propofol improves cardiac functional recovery after ischemia-reperfusion by upregulating nitric oxide synthase activity in the isolated rat hearts[J].Chin Med J (Engl),2009,122(24):3048-3054.
[6]
Chen J,Gu Y,Shao Z,et al.Propofol protects against hydrogen peroxide induced oxidative stress and cell dysfunction in human umbilical vein endothelial cells[J].Mol Cell Biochem,2010,339(12):43-54.
Kaminska B.MAPK signalling pathways as molecular targets for anti-inflammatory therapy—from molecular mechanisms to therapeutic benefits[J].Biochim Biophys Acta,2005,1754(1-2):253-262.
[12]
Motzkus D,Schulz-Maronde S,Heitland A,et al.The novel beta-defensin DEFB123 prevents lipopolysaccharide-mediated effects in vitro and in vivo[J].FASEB J,2006,20(10):1701-1702.
[13]
Dziarski R,Jin YP,Gupta D.Differential activation of extracellular signal-regulated kinase (ERK)1,ERK2,p38,and c-Jun NH2-terminal kinase mitogen-activated protein kinases by bacterial peptidoglyean[J].J Infect Dis,1996,174(4):777-785.
[14]
Murphy PG,Ogilvy AJ,Whiteley SM.The effect of propofol on the neutrophil respiratory burst[J].Eur J Anaesthesiol,1996,3(5):471-473.
[15]
Barrientos-Vega R,Mar Sánchez-Soria M,Morales-Garcia C,et al.Prolonged sedation of critically ill patients with midazolam or propofol:impact on weaning and costs[J].Crit Care Med,1997,25(1):33-40.