中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
8期
1829-1831
,共3页
杨林%钟明%李永继%莫陈程%汤礼军%黎冬暄
楊林%鐘明%李永繼%莫陳程%湯禮軍%黎鼕暄
양림%종명%리영계%막진정%탕례군%려동훤
急性胰腺炎%白细胞%鞘氨醇激酶-1%1-磷酸鞘氨醇
急性胰腺炎%白細胞%鞘氨醇激酶-1%1-燐痠鞘氨醇
급성이선염%백세포%초안순격매-1%1-린산초안순
Acute pancreatitis%Leucocyte%Sphingosine kinase 1%Sphingosine-1-phosphate
目的 观察人外周血白细胞中鞘氨醇激酶-1(SphK1)在急性胰腺炎(AP)的炎性反应中的作用.方法 选取30例AP患者,分为轻型急性胰腺炎(MAP)组17例和重型急性胰腺炎(SAP)组13例,另外纳入10例健康者作为健康对照组.在AP症状发生48、72 h 、5、7 d时分别检测血清肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6、外周血白细胞中SphK1 mRNA水平及其活性.结果 在48、72 h、5 d时,外周血白细胞中SphK1 mRNA及其活性均呈健康对照组＜MAP组＜SAP组(3组SphK1 mRNA的相对表达量:48 h:0.888±0.724、2.807±1.542、6.433±1.955;72 h:0.842±0.434、2.523±1.460、4.857±1.870;5 d:0.751±0.329、2.335±1.469、3.791±1.851; SphK1的活性:48 h:0.051 ±0.024、0.132 ±0.070、0.303±0.102;72 h:0.049 ±0.023、0.112±0.061、0.223 ±0.092;5 d:0.050 ±0.019、0.115 ±0.072、0.191±0.106,P ＜0.05);而且在48、72 h、5 d时,血清TNF-α、IL-6含量均呈健康对照组＜ MAP组＜SAP组[TNF-α(ng/L):48 h:4.72±1.69、17.48 ± 10.74、50.79±15.44;72 h:3.67 ±1.84、18.73 ±12.12、40.64±13.28;5 d:4.44 ±2.13、17.31±10.33、33.37±14.96;IL-6(ng/L):48 h:6.9±1.9、85.9±37.9、182.8±48.6;72 h:5.5 ±2.4、64.5 ±42.9、138.0±32.0;5 d:6.6±2.8、60.5 ±32.1、94.4 ±30.9,P＜0.05],这与外周血白细胞中SphK1的表达有相同的变化趋势.结论 SphK1的激活可能与AP的炎性反应密切相关.
目的 觀察人外週血白細胞中鞘氨醇激酶-1(SphK1)在急性胰腺炎(AP)的炎性反應中的作用.方法 選取30例AP患者,分為輕型急性胰腺炎(MAP)組17例和重型急性胰腺炎(SAP)組13例,另外納入10例健康者作為健康對照組.在AP癥狀髮生48、72 h 、5、7 d時分彆檢測血清腫瘤壞死因子(TNF)-α和白細胞介素(IL)-6、外週血白細胞中SphK1 mRNA水平及其活性.結果 在48、72 h、5 d時,外週血白細胞中SphK1 mRNA及其活性均呈健康對照組＜MAP組＜SAP組(3組SphK1 mRNA的相對錶達量:48 h:0.888±0.724、2.807±1.542、6.433±1.955;72 h:0.842±0.434、2.523±1.460、4.857±1.870;5 d:0.751±0.329、2.335±1.469、3.791±1.851; SphK1的活性:48 h:0.051 ±0.024、0.132 ±0.070、0.303±0.102;72 h:0.049 ±0.023、0.112±0.061、0.223 ±0.092;5 d:0.050 ±0.019、0.115 ±0.072、0.191±0.106,P ＜0.05);而且在48、72 h、5 d時,血清TNF-α、IL-6含量均呈健康對照組＜ MAP組＜SAP組[TNF-α(ng/L):48 h:4.72±1.69、17.48 ± 10.74、50.79±15.44;72 h:3.67 ±1.84、18.73 ±12.12、40.64±13.28;5 d:4.44 ±2.13、17.31±10.33、33.37±14.96;IL-6(ng/L):48 h:6.9±1.9、85.9±37.9、182.8±48.6;72 h:5.5 ±2.4、64.5 ±42.9、138.0±32.0;5 d:6.6±2.8、60.5 ±32.1、94.4 ±30.9,P＜0.05],這與外週血白細胞中SphK1的錶達有相同的變化趨勢.結論 SphK1的激活可能與AP的炎性反應密切相關.
목적 관찰인외주혈백세포중초안순격매-1(SphK1)재급성이선염(AP)적염성반응중적작용.방법 선취30례AP환자,분위경형급성이선염(MAP)조17례화중형급성이선염(SAP)조13례,령외납입10례건강자작위건강대조조.재AP증상발생48、72 h 、5、7 d시분별검측혈청종류배사인자(TNF)-α화백세포개소(IL)-6、외주혈백세포중SphK1 mRNA수평급기활성.결과 재48、72 h、5 d시,외주혈백세포중SphK1 mRNA급기활성균정건강대조조＜MAP조＜SAP조(3조SphK1 mRNA적상대표체량:48 h:0.888±0.724、2.807±1.542、6.433±1.955;72 h:0.842±0.434、2.523±1.460、4.857±1.870;5 d:0.751±0.329、2.335±1.469、3.791±1.851; SphK1적활성:48 h:0.051 ±0.024、0.132 ±0.070、0.303±0.102;72 h:0.049 ±0.023、0.112±0.061、0.223 ±0.092;5 d:0.050 ±0.019、0.115 ±0.072、0.191±0.106,P ＜0.05);이차재48、72 h、5 d시,혈청TNF-α、IL-6함량균정건강대조조＜ MAP조＜SAP조[TNF-α(ng/L):48 h:4.72±1.69、17.48 ± 10.74、50.79±15.44;72 h:3.67 ±1.84、18.73 ±12.12、40.64±13.28;5 d:4.44 ±2.13、17.31±10.33、33.37±14.96;IL-6(ng/L):48 h:6.9±1.9、85.9±37.9、182.8±48.6;72 h:5.5 ±2.4、64.5 ±42.9、138.0±32.0;5 d:6.6±2.8、60.5 ±32.1、94.4 ±30.9,P＜0.05],저여외주혈백세포중SphK1적표체유상동적변화추세.결론 SphK1적격활가능여AP적염성반응밀절상관.
Objective To investigate the role of sphingosine kinase 1 (SphK1) of peripheral blood leucocytes in inflammatory response in the patients with acute pancreatitis (AP).Methods Thirty patients with AP were enrolled and divided into severe AP (SAP) group (n =13) and mild acute AP (MAP) group (n =17).Ten healthy volunteers were selected as healthy control group.The serum levels of tumor necrosis factor (TNF)-α,interleukin (IL)-6,and the expression levels of SphK1 mRNA and enzymatic activity of peripheral blood leucocytes were detected at 48 h,72 h,5 day,and 7 day after the attack of AP.Results At 48 h,72 h and 5 day,the expression levels of SphK1 mRNA and enzymatic activity of peripheral blood leucocytes were the lowest in healthy control group,followed by MAP group and SAP group (the expression of SphK1 mRNA:48 h,0.888 ± 0.724 vs.2.807 ± 1.542 vs.6.433 ± 1.955 ; 72 h,0.842 ± 0.434 vs.2.523 ± 1.460 vs.4.857 ± 1.870; 5 day,0.751 ± 0.329 vs.2.335 ± 1.469 vs.3.791 ± 1.851; SphK1 enzymatic activity:48 h,0.051 ±0.024 vs.0.132 ±0.070 vs.0.303 ± 0.102; 72 h,0.049 ±0.023 vs.0.112 ±0.061 vs.0.223 ±0.092; 5 day,0.050 ±0.019 vs.0.115 ± 0.072 vs.0.191 ±0.106,P ＜ 0.05).At 48,72 h and 5 d,the concentrations of serum TNF-α and IL-6 were lowest in healthy control group,followed by MAP and SAP groups [TNF-α (ng/L):48 h:4.72 ± 1.69 vs.17.48 ±10.74 vs.50.79±15.44; 72h:3.67 ±1.84 vs.18.73 ±12.12 vs.40.64 ±13.28; 5d:4.44±2.13 vs.17.31 ±10.33 vs.33.37 ±14.96; IL-6 (ng/L):48 h:6.9±1.9 vs.85.9±37.9 vs.182.8 ±48.6; 72h:5.5 ±2.4 vs.64.5 ±42.9 vs.138.0±32.0;5 d:6.6±2.8 vs.60.5 ±32.1 vs.94.4 ± 30.9,P ＜ 0.05].The levels of serum TNF-α and IL-6 showed similar shift with intracellular SphK1 expression.Conclusion Activated SphK1 may be implicated in inflammatory response in AP.
