中华普通外科杂志
中華普通外科雜誌
중화보통외과잡지
CHINESE JOURNAL OF GENERAL SURGERY
2013年
5期
382-385
,共4页
李纾%朱凤雪%李晖%张洪斌%安友仲
李紓%硃鳳雪%李暉%張洪斌%安友仲
리서%주봉설%리휘%장홍빈%안우중
再灌注损伤%T淋巴细胞,调节性%白细胞介素33
再灌註損傷%T淋巴細胞,調節性%白細胞介素33
재관주손상%T림파세포,조절성%백세포개소33
Reperfusion injury%T lymphocyte,regulatory%Interleukin-33
目的 研究白细胞介素(interleukin,IL)-33对小鼠肝热缺血再灌注(ischemia/reperfusion,I/R)损伤的保护作用,寻求缓解肝I/R损伤的有效方法.方法 采用小鼠肝脏热缺血再灌注损伤模型.首先检测小鼠肝脏I/R损伤时IL-33的mRNA和蛋白水平的变化.小鼠分对照组、模型组、重组IL-33干预组和抗ST2L抗体干预组,检测I/R损伤6h后天冬氨酸转氨酶(aspartateaminotransferase,AST)和丙氨酸转氨酶(alanine aminotransferase,ALT)水平、肝组织病理变化和血清肿瘤坏死因子(tumor necrosis factor,TNF)-α、干扰素(interferon,IFN)-γ、IL-4、IL-5、IL-13水平.结果 肝脏I/R损伤时,IL-33的mRNA和蛋白水平水平显著升高(t再灌注2h=-3.574,t再灌注6 h=-4.147; P<0.05).重组IL-33干预后小鼠血清肝酶水平明显下降(tALT=4.592,tAST=3.471;P<0.05),病理损伤程度减轻,IL-4、IL-5、IL-13水平升高(tIL-4=-4.995,tIL-5=-4.584,tIL-13=-4.431;P<0.05),IFN-γ,水平下降(t=5.402,P<0.05).抗ST2L抗体干预则有相反的作用.IL-33组和抗ST2L抗体组小鼠的血清TNF-α水平与模型组相比,差异无统计学意义(tTNF-α=0.261,P >0.05).结论 小鼠肝脏热缺血再灌注损伤时IL-33mRNA及血清蛋白表达水平显著增高,对发生I/R损伤的肝脏发挥保护作用,其机制可能与促进Th1/Th2平衡向后者偏移有关.
目的 研究白細胞介素(interleukin,IL)-33對小鼠肝熱缺血再灌註(ischemia/reperfusion,I/R)損傷的保護作用,尋求緩解肝I/R損傷的有效方法.方法 採用小鼠肝髒熱缺血再灌註損傷模型.首先檢測小鼠肝髒I/R損傷時IL-33的mRNA和蛋白水平的變化.小鼠分對照組、模型組、重組IL-33榦預組和抗ST2L抗體榦預組,檢測I/R損傷6h後天鼕氨痠轉氨酶(aspartateaminotransferase,AST)和丙氨痠轉氨酶(alanine aminotransferase,ALT)水平、肝組織病理變化和血清腫瘤壞死因子(tumor necrosis factor,TNF)-α、榦擾素(interferon,IFN)-γ、IL-4、IL-5、IL-13水平.結果 肝髒I/R損傷時,IL-33的mRNA和蛋白水平水平顯著升高(t再灌註2h=-3.574,t再灌註6 h=-4.147; P<0.05).重組IL-33榦預後小鼠血清肝酶水平明顯下降(tALT=4.592,tAST=3.471;P<0.05),病理損傷程度減輕,IL-4、IL-5、IL-13水平升高(tIL-4=-4.995,tIL-5=-4.584,tIL-13=-4.431;P<0.05),IFN-γ,水平下降(t=5.402,P<0.05).抗ST2L抗體榦預則有相反的作用.IL-33組和抗ST2L抗體組小鼠的血清TNF-α水平與模型組相比,差異無統計學意義(tTNF-α=0.261,P >0.05).結論 小鼠肝髒熱缺血再灌註損傷時IL-33mRNA及血清蛋白錶達水平顯著增高,對髮生I/R損傷的肝髒髮揮保護作用,其機製可能與促進Th1/Th2平衡嚮後者偏移有關.
목적 연구백세포개소(interleukin,IL)-33대소서간열결혈재관주(ischemia/reperfusion,I/R)손상적보호작용,심구완해간I/R손상적유효방법.방법 채용소서간장열결혈재관주손상모형.수선검측소서간장I/R손상시IL-33적mRNA화단백수평적변화.소서분대조조、모형조、중조IL-33간예조화항ST2L항체간예조,검측I/R손상6h후천동안산전안매(aspartateaminotransferase,AST)화병안산전안매(alanine aminotransferase,ALT)수평、간조직병리변화화혈청종류배사인자(tumor necrosis factor,TNF)-α、간우소(interferon,IFN)-γ、IL-4、IL-5、IL-13수평.결과 간장I/R손상시,IL-33적mRNA화단백수평수평현저승고(t재관주2h=-3.574,t재관주6 h=-4.147; P<0.05).중조IL-33간예후소서혈청간매수평명현하강(tALT=4.592,tAST=3.471;P<0.05),병리손상정도감경,IL-4、IL-5、IL-13수평승고(tIL-4=-4.995,tIL-5=-4.584,tIL-13=-4.431;P<0.05),IFN-γ,수평하강(t=5.402,P<0.05).항ST2L항체간예칙유상반적작용.IL-33조화항ST2L항체조소서적혈청TNF-α수평여모형조상비,차이무통계학의의(tTNF-α=0.261,P >0.05).결론 소서간장열결혈재관주손상시IL-33mRNA급혈청단백표체수평현저증고,대발생I/R손상적간장발휘보호작용,기궤제가능여촉진Th1/Th2평형향후자편이유관.
Objective To study the protective effect of interleukin-33 (IL-33) on mouse warm hepatic ischemia-reperfusion (I/R) injury.Methods On a mouse warm hepatic I/R injury model IL-33 mRNA and protein levels during hepatic ischemia and reperfusion period were determined,and then mice were divided into control group,model group,recombinant IL-33 intervention group and anti ST2L antibody intervention group,and mice were sacrificed after 6 hours of reperfusion.Serum aspartate aminotransferase (AST),alanine aminotransferase (ALT) protein levels were determined.Liver pathology was observed by transmission electron microscopy and serum cytokine level (tumor necrosis factor-α,interferon-γ,IL-4,IL-5,IL-13) were measured by flow cytometry CBA method.Results The level of IL-33 mRNA and protein were significantly higher in the reperfusion stage (t2 h =-3.574,t6 h =-4.147 ; P < 0.05).After intervention by recombinant IL-33,the level of serum ALT and AST decreased significantly (tALT =4.592,tAST =3.471 ; P < 0.05),the severity of pathological damage was reduced,the levels of IL-4,IL-5,IL-13 increased and that of IFN-γ decreased,with statistically significant difference in comparison with the control groups (tIL-4 =-4.995,tIL-5 =-4.584,tIL-13 =-4.431 ; P < 0.05).Anti-ST2L antibody intervention effected the opposite.Serum TNF-α level did not change in intervention groups compared with that in model group (tTNF-α =0.261,P > 0.05).Conclusions IL-33 mRNA and protein level increased in mice with hepatic I/P injury.IL-33 exerts a protective effect on the I/R injured liver after binding to its receptor ST2L.