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作 者:曹俊[1] 魏珂[1] 李庆姝[2] 黎平[1] 董军[1] 罗洁[1] 程波[1] 闵苏[1]
机构地区:[1]重庆医科大学附属第一医院麻醉科,400016 [2]重庆医科大学病理科
出 处:《中华麻醉学杂志》2013年第11期1397-1400,共4页Chinese Journal of Anesthesiology
基 金:国家临床重点专科建设项目(财社[2011]170号);重庆市临床重点学科项目(渝卫科教[2007]2号)
摘 要: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20~25g,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45min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PC61250μg。IRI组和P组于再灌注24h(T1)和72h(T2)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1RI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L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。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 IRt and anti-CD25 monoclonal antibody PC61 group (group P). Bilateral kidneys were exposed and their pedicles were occluded for 45 min with atraumatic mini- clamp followed by 72 h reperfusion. PC61 250μg was injected intraperitoneally at 24 h before the model was estab- lished. Blood samples were collected from the inferior vena cava at 24 and 72 h of reperfusion (T1-2) for determi- nation 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. Re- suits Compared with group S, the serum BUN and Cr concentrations and pathological scores were significantly in- creased 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 concentra- tions 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 Tl and T2 in group P ( P 〉 0.05). Conclusion Tregs are endogenous regu-latory factors during renal ischemia-reperfusion, are helpful in inhibiting the inflammatory response and reduce IRI in mice.
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