中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2012年
6期
392-395
,共4页
张海峰%吴兴%丁晓凌%强晖%曹维%陈海琴%周国雄
張海峰%吳興%丁曉凌%彊暉%曹維%陳海琴%週國雄
장해봉%오흥%정효릉%강휘%조유%진해금%주국웅
胰腺炎,急性坏死性%趋化因子类%CXCL11
胰腺炎,急性壞死性%趨化因子類%CXCL11
이선염,급성배사성%추화인자류%CXCL11
Pancreatitis,acute ncerotizing%Chemokines,CXC%CXCL11
目的 观察趋化因子CXCL11在急性坏死性胰腺炎(ANP)病程中的动态变化,探讨其在ANP发病过程中的作用.方法 48只SD大鼠按数字表法随机分为对照组和ANP组,每组24只.采用4%牛黄胆酸钠(1 ml/kg体重)逆行胰胆管注射方法制备ANP大鼠模型.术后1、3、6、12 h处死大鼠,留取标本.检测血清淀粉酶活性,胰腺组织行常规病理检查并评分,免疫组化法检测胰腺组织CXCL11表达,定量PCR法检测胰腺组织CXCL11 mRNA表达,酶联免疫吸附试验法检测血清CXCL11水平.结果 ANP组大鼠血清淀粉酶活性较对照组显著升高[6h时为(6153±355)U/L比(185±32)U/L,P<0.05];胰腺病理损伤明显,病理评分较对照组显著增加[6h时为(9.00±0.63)分比(0.33±0.12)分,P<0.05];胰腺组织CXCL11 mRNA及蛋白表达较对照组显著增强(6h时为3.13±0.43比0.99±0.24,2.76±0.27比0.33±0.12,P值均<0.05);血清CXCL11水平较对照组明显升高[6h时为(112.1±14.2)ng/L比(56.8 4.3) ng/L,P<0.05].结论 CXCL11是急性胰腺炎早期的炎症介质,参与了大鼠ANP的发病过程.
目的 觀察趨化因子CXCL11在急性壞死性胰腺炎(ANP)病程中的動態變化,探討其在ANP髮病過程中的作用.方法 48隻SD大鼠按數字錶法隨機分為對照組和ANP組,每組24隻.採用4%牛黃膽痠鈉(1 ml/kg體重)逆行胰膽管註射方法製備ANP大鼠模型.術後1、3、6、12 h處死大鼠,留取標本.檢測血清澱粉酶活性,胰腺組織行常規病理檢查併評分,免疫組化法檢測胰腺組織CXCL11錶達,定量PCR法檢測胰腺組織CXCL11 mRNA錶達,酶聯免疫吸附試驗法檢測血清CXCL11水平.結果 ANP組大鼠血清澱粉酶活性較對照組顯著升高[6h時為(6153±355)U/L比(185±32)U/L,P<0.05];胰腺病理損傷明顯,病理評分較對照組顯著增加[6h時為(9.00±0.63)分比(0.33±0.12)分,P<0.05];胰腺組織CXCL11 mRNA及蛋白錶達較對照組顯著增彊(6h時為3.13±0.43比0.99±0.24,2.76±0.27比0.33±0.12,P值均<0.05);血清CXCL11水平較對照組明顯升高[6h時為(112.1±14.2)ng/L比(56.8 4.3) ng/L,P<0.05].結論 CXCL11是急性胰腺炎早期的炎癥介質,參與瞭大鼠ANP的髮病過程.
목적 관찰추화인자CXCL11재급성배사성이선염(ANP)병정중적동태변화,탐토기재ANP발병과정중적작용.방법 48지SD대서안수자표법수궤분위대조조화ANP조,매조24지.채용4%우황담산납(1 ml/kg체중)역행이담관주사방법제비ANP대서모형.술후1、3、6、12 h처사대서,류취표본.검측혈청정분매활성,이선조직행상규병리검사병평분,면역조화법검측이선조직CXCL11표체,정량PCR법검측이선조직CXCL11 mRNA표체,매련면역흡부시험법검측혈청CXCL11수평.결과 ANP조대서혈청정분매활성교대조조현저승고[6h시위(6153±355)U/L비(185±32)U/L,P<0.05];이선병리손상명현,병리평분교대조조현저증가[6h시위(9.00±0.63)분비(0.33±0.12)분,P<0.05];이선조직CXCL11 mRNA급단백표체교대조조현저증강(6h시위3.13±0.43비0.99±0.24,2.76±0.27비0.33±0.12,P치균<0.05);혈청CXCL11수평교대조조명현승고[6h시위(112.1±14.2)ng/L비(56.8 4.3) ng/L,P<0.05].결론 CXCL11시급성이선염조기적염증개질,삼여료대서ANP적발병과정.
Objective To investigate the dynamic expressions of CXCL11 and its role in the pathogenesis of acute necrotizing pancreatitis (ANP).Methods Forty-eight SD rats were randomly divided into control group and ANP group,with 24 rats in each group.ANP model was induced by retrograde injection of 4% sodium taurocholate (1 ml/kg body weight) into the biliary and pancreatic duct.The rats were sacrificed at 1,3,6,12 hours.Serum level of amylase was determined,pathological changes in pancreatic tissue were routinely observed and scored.The expression of CXCL11 mRNA and proteon in pancreas was measured by fluorescence quantitative polymerase chain reaction and immunohistochemical method.The serum levels of CXCL11 were measured by enzyme-linked immunoadsorbent assay.Results The serum levels of amylase in ANP rats were significantly higher than those in control group [(6153 ± 355)U/L vs (185 ± 32)U/L at 6 h,P <0.05],pathological changes in pancreatre tisues were more significant in ANP rats,and the pathological score was significantly higher than that in control group [(9.00 ± 0.63) vs (0.33 ± 0.12) points at 6 h,P < 0.05] ; the expressions of CXCL11 mRNA and protein in pancreatic tissue were significantly increased than those in control group (3.13 ± 0.43 vs 0.99 ± 0.24,2.76 ± 0.27 vs 0.33 ± 0.12 at 6 h,P < 0.05).The serum level of CXCL11 was significantly higher than that in control group [(112.1 ± 14.2)ng/L vs (56.8 ±4.3) ng/L at 6 h,P <0.05)].Conclusions CXCL11 is an early inflammatory mediator in acute pancreatitis,and involved in the pathogenesis of ANP in rats.