CAJ | 학술논문

目的：探讨重组旋毛虫蛋白rTsP38对小鼠肠缺血/再灌注( I/R)损伤的保护效应,并从巨噬细胞角度初步探讨其机制。方法 BALB/c小鼠随机分为假手术组( S组)、肠I/R伤组( I组)、rTsP38免疫组( T组)和佐剂免疫组( A组)。建立I/R模型前6周,分别给予下述试剂,共3次,每次间隔14 d。 S组和I组予PBS 0.2 ml,T组予rTsP380.2 ml(含25μg与等体积弗氏完全或不完全佐剂乳化混匀的rTsP38),A组予0.1 ml PBS+0.1 ml弗氏完全或不完全佐剂。结果 I组小鼠肠黏膜损伤严重,改良Chiu's评分明显增高,中性粒细胞明显增多,进食量和体重均明显下降,M2型巨噬细胞标志物Arg-1表达下降,M1型巨噬细胞NOS2表达增加。 T组小鼠血清IgG1明显升高( P<0.01),改良Chiu's评分明显降低,中性粒细胞明显减少,细胞增殖明显增多,绒毛高度明显增高,进食量和体重均明显增加,Arg-1和NOS2表达均明显增高,且以Arg-1为主。结论 rTsP38促进Th2型免疫反应和M1向M2型巨噬细胞转变,从而减轻小鼠肠I/R所致肠损伤,促进肠黏膜修复和肠功能恢复。
목적：탐토중조선모충단백rTsP38대소서장결혈/재관주( I/R)손상적보호효응,병종거서세포각도초보탐토기궤제。방법 BALB/c소서수궤분위가수술조( S조)、장I/R상조( I조)、rTsP38면역조( T조)화좌제면역조( A조)。건립I/R모형전6주,분별급여하술시제,공3차,매차간격14 d。 S조화I조여PBS 0.2 ml,T조여rTsP380.2 ml(함25μg여등체적불씨완전혹불완전좌제유화혼균적rTsP38),A조여0.1 ml PBS+0.1 ml불씨완전혹불완전좌제。결과 I조소서장점막손상엄중,개량Chiu's평분명현증고,중성립세포명현증다,진식량화체중균명현하강,M2형거서세포표지물Arg-1표체하강,M1형거서세포NOS2표체증가。 T조소서혈청IgG1명현승고( P<0.01),개량Chiu's평분명현강저,중성립세포명현감소,세포증식명현증다,융모고도명현증고,진식량화체중균명현증가,Arg-1화NOS2표체균명현증고,차이Arg-1위주。결론 rTsP38촉진Th2형면역반응화M1향M2형거서세포전변,종이감경소서장I/R소치장손상,촉진장점막수복화장공능회복。
Aim To investigate the the protective effects of a novel recombinant Trichinella spiralis 38 ku protein ( rTsP38 ) on intestinal I/R injury and the po-tential mechanisms. Methods Male BALB/c mice were randomly divided into sham group ( group S) , in-jury group ( group I) , rTsP38 vaccinated group ( group T) and adjuvants vaccinated group ( group A ) , and received subcutaneously phosphate buffer solution (PBS), PBS, rTsP38, or adjuvants, respectively, at 2-week intervals 6 weeks before the surgical proce-dure. Results Intestinal I/R caused severe intestinal injury evidenced by significant increases in modified Chiu 's score and neutrophils infiltration, accompanied by decreases in daily food intake and body weight. The mRNA level of arginase-1 ( Arg-1 ) was decreased and the mRNA level of inducible nitric oxide synthase 2 ( NOS2) was increased in group I. RTsP38 significant-ly ameliorated intestinal injury and improved intestinal function following intestinal I/R accompanied by de-crease in neutrophils infiltration and increase in cell proliferation in the intestine, compared to mice without rTsP38 pretreatment. Fold changes of Arg-1 mRNA level were significantly increased in group T. Conclu-sions These findings indicate that rTsP38 exerts pro-tection on intestinal I/R injury in mice via promoting M2 macrophages polarization.