CAJ | 학술논문

目的探讨调节性T淋巴细胞(Treg细胞)在小鼠肾缺血再灌注损伤中的作用.方法雄性SPF级C57BL/6小鼠48只,8～ 12周龄,体重20 ～ 25 g,采用随机数字表法,将其分为3组(n=16):假手术组(S组)、肾缺血再灌注损伤组(IRI组)和CD25单克隆抗体PC61组(P组).采用阻断双侧肾蒂45 min再灌注法制备肾脏缺血再灌注损伤.P组于模型制备前24h腹腔注射PC61 250μg.IRI组和P组于再灌注24 h(T1)和72 h(T)时、S组于相应时点取下腔静脉血样,测定血清BUN、Cr浓度,随后取双肾,进行肾组织损伤评分和测定Treg细胞数量.结果与S组比较,T1,2时IRI组和P组血清BUN、Cr浓度和肾组织病理学评分升高,IRI组肾组织Treg细胞数量增加,P组肾组织Treg细胞数量减少(P＜0.05);与IRI组比较,T2时P组血清BUN、Cr浓度和肾组织病理学评分升高,T1,2时肾组织Treg细胞数量减少(P＜0.05);与T1时比较,IRI组T2时血清BUN、Cr浓度和肾组织病理学评分降低,肾组织Treg细胞数量增加(P＜0.05),P组T2时上述指标差异无统计学意义(P＞0.05).结论 Treg细胞为小鼠肾缺血再灌注时的内源性调节因子,有助于抑制炎症反应,减轻缺血再灌注损伤.
목적 탐토조절성T림파세포(Treg세포)재소서신결혈재관주손상중적작용.방법 웅성SPF급C57BL/6소서48지,8～ 12주령,체중20 ～ 25 g,채용수궤수자표법,장기분위3조(n=16):가수술조(S조)、신결혈재관주손상조(IRI조)화CD25단극륭항체PC61조(P조).채용조단쌍측신체45 min재관주법제비신장결혈재관주손상.P조우모형제비전24h복강주사PC61 250μg.IRI조화P조우재관주24 h(T1)화72 h(T)시、S조우상응시점취하강정맥혈양,측정혈청BUN、Cr농도,수후취쌍신,진행신조직손상평분화측정Treg세포수량.결과 여S조비교,T1,2시IRI조화P조혈청BUN、Cr농도화신조직병이학평분승고,IRI조신조직Treg세포수량증가,P조신조직Treg세포수량감소(P＜0.05);여IRI조비교,T2시P조혈청BUN、Cr농도화신조직병이학평분승고,T1,2시신조직Treg세포수량감소(P＜0.05);여T1시비교,IRI조T2시혈청BUN、Cr농도화신조직병이학평분강저,신조직Treg세포수량증가(P＜0.05),P조T2시상술지표차이무통계학의의(P＞0.05).결론 Treg세포위소서신결혈재관주시적내원성조절인자,유조우억제염증반응,감경결혈재관주손상.
Objective To evaluate the role of regulatory T cells (Tregs) in the renal ischemia-reperfusion injury (IRI) in mice.Methods Forty-eight male C57BL/6J mice,weighing 20-25 g,were randomly divided into 3 groups (n =16 each):sham operation group (group S),group IRI and anti-CD25 monoclonal antibody PC61 group (group P).Bilateral kidneys were exposed and their pedicles were occluded for 45 min with atraumatic miniclamp followed by 72 h reperfusion.PC61 250 μg was injected intraperitoneally at 24 h before the model was established.Blood samples were collected from the inferior vena cava at 24 and 72 h of reperfusion (T1,2) for determination of serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations.Bilateral kidneys were obtained for determination of the number of Tregs in renal tissues and the pathological changes of the kidney were scored.Results Compared with group S,the serum BUN and Cr concentrations and pathological scores were significantly increased at T1,2 in IRI and P groups,the number of Tregs was increased at T1,2 in IRI group,and the number of Tregs was decreased at T1,2 in P group (P ＜ 0.05).Compared with group IRI,the serum BUN and Cr concentrations and pathological scores were significantly increased at T2,and the number of Tregs was decreased at T1,2 in P group (P ＜ 0.05).The serum BUN and Cr concentrations and pathological scores were significantly lower,and the number of Tregs was larger at T2 than at T1 in group IRI (P ＜ 0.05).There was no significant difference in the parameters mentioned above between T1 and T2 in group P (P ＞ 0.05).Conclusion Tregs are endogenous regulatory factors during renal ischemia-reperfusion,are helpful in inhibiting the inflammatory response and reduce IRI in mice.