CAJ | 학술논문

目的探讨巴利昔单抗(Basiliximab)预处理对小鼠肾脏缺血再灌注损伤(IRI)的影响及其机制.方法将54只健康雄性C57BL/6小鼠随机分为3组(n=18).假手术组(Sham组):仅行开腹及双侧肾蒂分离;缺血再灌注对照组(IR组):术前30 min经尾静脉注射非特异性IgG(1 mg/kg)后,夹闭双肾蒂45 min;巴利昔单抗组(Basiliximab组):术前30 min经尾静脉注射巴利昔单抗(1 mg/kg)后,夹闭双肾蒂45 min.各组小鼠于再灌注1、4、24 h后取其血、尿液检测血肌酐(Scr)、血尿素氮(BUN)、肾小球滤过钠排泄分数(FENa,％);取肾组织行病理学检查;流式细胞仪检测小鼠肾脏中CD4+T淋巴细胞及CD8+T淋巴细胞含量;逆转录-聚合酶链反应(RT-PCR)检测白细胞介素(IL)-2、肿瘤坏死因子-α(TNF-α)、IL-6表达量.结果与Sham组比较,再灌注24 h后,小鼠血清Ser、BUN水平在IR组[(174.33±7.69)、(69.90±1.68) μmol/L]和Basiliximab组[(51.67±6.56)、(23.97±2.12) μmol/L]明显升高(P ＜0.05);FENa明显升高(P＜0.05);肾组织损伤及评分均升高(P＜0.05),肾组织内IL-2、TNF-α、IL-6表达量升高(P＜0.05);与Sham组比较,再灌注4h后,小鼠肾脏CD4+T淋巴细胞含量在IR组和Basiliximab组均升高(P＜0.05).其中上述指标在Basiliximab组水平较IR组均明显降低(P＜0.05).结论巴利昔单抗预处理可减轻小鼠肾脏IRI,其机制可能是抑制小鼠肾脏IRI早期浸润CD4+T淋巴细胞增殖后减少相关炎性因子聚集,从而减轻炎性损伤.
목적 탐토파리석단항(Basiliximab)예처리대소서신장결혈재관주손상(IRI)적영향급기궤제.방법 장54지건강웅성C57BL/6소서수궤분위3조(n=18).가수술조(Sham조):부행개복급쌍측신체분리;결혈재관주대조조(IR조):술전30 min경미정맥주사비특이성IgG(1 mg/kg)후,협폐쌍신체45 min;파리석단항조(Basiliximab조):술전30 min경미정맥주사파리석단항(1 mg/kg)후,협폐쌍신체45 min.각조소서우재관주1、4、24 h후취기혈、뇨액검측혈기항(Scr)、혈뇨소담(BUN)、신소구려과납배설분수(FENa,％);취신조직행병이학검사;류식세포의검측소서신장중CD4+T림파세포급CD8+T림파세포함량;역전록-취합매련반응(RT-PCR)검측백세포개소(IL)-2、종류배사인자-α(TNF-α)、IL-6표체량.결과 여Sham조비교,재관주24 h후,소서혈청Ser、BUN수평재IR조[(174.33±7.69)、(69.90±1.68) μmol/L]화Basiliximab조[(51.67±6.56)、(23.97±2.12) μmol/L]명현승고(P ＜0.05);FENa명현승고(P＜0.05);신조직손상급평분균승고(P＜0.05),신조직내IL-2、TNF-α、IL-6표체량승고(P＜0.05);여Sham조비교,재관주4h후,소서신장CD4+T림파세포함량재IR조화Basiliximab조균승고(P＜0.05).기중상술지표재Basiliximab조수평교IR조균명현강저(P＜0.05).결론 파리석단항예처리가감경소서신장IRI,기궤제가능시억제소서신장IRI조기침윤CD4+T림파세포증식후감소상관염성인자취집,종이감경염성손상.
Objective To investigate the effect and mechanism of basiliximab preconditioning on renal ischemia/reperfusion injury.Methods Fifty-four C57BL/6 mice were divided into three groups randomly:sham-operated group (Sham group) ; ischemia/reperfusion group (IR group) [mice were injected with non-specific IgG (1 mg/kg) via tail vein 30 min before the operation] ; preconditioning with basiliximab group (Basiliximab group) [mice were injected with basiliximab (1 mg/kg) via tail vein 30 min before the operation].Then we occluded the renal pedicles on both sides for 45 min.Serum creatinine (Scr),blood urea nitrogen (BUN),fractional excretion of sodium (FENa),renal histology,CD4 + T lymphocytes,CD8 +T lymphocytes,interleukin (IL)-2,tumor necrosis factor (TNF)-α,and IL-6 in blood or the kidney were examined after reperfusion for 1,4,24 h.Results Compared with the Sham group,the levels of Scr [(174.33 ± 7.69),and (51.67 ± 6.56) μmol/L],BUN [(69.90 ± 1.68),and (23.97 ± 2.12) μ mol/L],FENa,the pathological injury scores,IL-2,TNF-α,and IL-6 were increased significantly in IR group and Basiliximab group after reperfusion for 24 h.CD4 + T lymphocytes were also increased in Basiliximab and IR groups after reperfusion for 4 h.All these variables were significantly decreased in Basiliximab group as compared with IR group.Conclusion Preconditioning with basiliximab alleviated renal ischemia/reperfusion injury probably by inhibiting CD4 +T lymphocytes proliferation and decreasing the expression of pro-inflammatory cytokines.