牛磺酸和环孢素A对氯化锰致大鼠肝脏线粒体氧化损伤作用的影响

王建军; 贾克

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牛磺酸和环孢素A对氯化锰致大鼠肝脏线粒体氧化损伤作用的影响

王建军 , 贾克

文章导航 > 蚌埠医学院学报 > 2010, 35 > 12: (1217-1219)

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牛磺酸和环孢素A对氯化锰致大鼠肝脏线粒体氧化损伤作用的影响

王建军,
贾克

蚌埠医学院卫生学教研室, 安徽蚌埠 233030

作者简介: 王建军(1984-),男,助教.

基金项目:
蚌埠医学院科研资助项目(BY0834)
中图分类号: R595.2

Effect of taurine and cyclosporine A on oxidative damage of liver mitochondrial induced by manganese chloride in rats

Department of Hygiology, Bengbu Medical College, Bengbu Anhui 233030, China
CLC number: R595.2

摘要: 目的:观察牛磺酸(taurine,Tau)和环孢素A(cyclosporine A,CSA)对锰(Mn)致大鼠肝脏线粒体氧化损伤作用的影响,并探讨Mn致肝脏毒性的细胞分子学机制。方法:24只雄性SD大鼠按体重随机均分为4组。第1组为对照组,皮下注射生理盐水;第2组为单纯染Mn(MnCl₂)组,皮下注射生理盐水;第3、4组为预处理(Tau+MnCl₂组和CSA+MnCl₂组),分别皮下注射Tau(100 mg/kg)和CSA(1 mg/kg)。皮下注射2 h后,第1组腹腔注射生理盐水,第2~4组腹腔注射MnCl₂溶液(32 mg/kg),染Mn 30天,Tau和CSA隔日注射1次,共干预15次。最后1次染Mn后24 h,切取肝组织。测定肝线粒体膜肿胀度、膜电位、PT孔和SDH活性、细胞色素C含量以及GSH-PX活性、OH.含量。结果:大鼠单纯染Mn 30天后,与对照组比较线粒体膜肿胀度光密度降低(P<0.05),PT孔、线粒体膜电位光密度降低,GSH-PX和SDH活性降低,细胞色素C和OH.含量升高(P<0.05~P<0.01);Tau+MnCl₂组与MnCl₂组相比,线粒体膜肿胀度光密度、PT孔、线粒体膜电位光密度升高(P<0.05~P<0.01),GSH-PX和SDH活性升高,细胞色素C和OH.含量降低(P<0.01);CSA+MnCl₂组与MnCl₂组相比,PT孔、线粒体膜电位光密度升高,GSH-PX和SDH活性升高,细胞色素C含量降低(P<0.01)。结论:Tau和CSA对Mn引起的肝脏线粒体氧化损伤有不同程度的拮抗作用。
- 锰 /
- 牛磺酸 /
- 环孢素A /
- 线粒体 /
- 氧化应激 /
- 大鼠
Abstract: Objective: To study the effect of different doses of manganese (Mn) on oxidative damage of liver mitochondrial induced by Mn chloride,and to explore the cell molecular mechanism of Mn-induced exeitotoxicity.Methods: Twenty four male SD rats were randomly divided into four groups by weight.The first group (control group) were given subcutaneous injection of physiological saline only;the second group (Mn-exposed group) were injected 32 mg/kg of MnCl₂ subcutaneously;the third and fourth groups were intraperitoneally injected 100 mg/kg of taurine (Tau) and 1 mg/kg of cyclosporine A (CSA),respectively.Two hours after subcutaneous injection,the first group were intraperitoneally injected physiological saline,and the other three groups received intraperitoneal injection of 32 mg/kg of MnCl₂ for 30 days,and Tau and CSA were injected every other day for 15 times.At the 24th hour after the last administration of MnCl₂,the rats were killed and the liver was taken to detect the mitochondrial swelling amplitude,mitochondrial membrane potential (MMP),permeability transition pore (PT pore),the activity of GSH-PX,SDH and the content of cytochrome C and OH·.Results: Compared with control group,the mitochondrial swelling amplitude,PT pore,MMP,the activity of GSH-PX and SDH decreased in the MnCl₂ group,while the content of cytochrome C and OH·increased (P<0.05 to P<0.01).Compared with MnCl₂ group,the mitochondrial swelling amplitude,PT pore and MMP increased in Tau pretreatment group (P<0.05 to P<0.01),while the activity of GSH-PX and SDH increased,and the content of cytochrome C and OH·decreased (P<0.01).Compared with control group,the activity of GSH-PX and SDH,PT pore and MMP increased in CSA pretreatment group,while the content of cytochrome C decreased (P<0.01).Conclusions: Tau and CSA have some antagonistic effects on oxidative damage of liver mitochondrial induced by manganese.
- manganese /
- taurine /
- cyclosporine A /
- mitochondrial /
- oxidative stress /
- rats

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牛磺酸和环孢素A对氯化锰致大鼠肝脏线粒体氧化损伤作用的影响

王建军
贾克

作者简介: 王建军(1984-),男,助教.

蚌埠医学院卫生学教研室, 安徽蚌埠 233030

收稿日期: 2010-05-10

基金项目: 蚌埠医学院科研资助项目(BY0834)

关键词:

摘要: 目的:观察牛磺酸(taurine,Tau)和环孢素A(cyclosporine A,CSA)对锰(Mn)致大鼠肝脏线粒体氧化损伤作用的影响,并探讨Mn致肝脏毒性的细胞分子学机制。方法:24只雄性SD大鼠按体重随机均分为4组。第1组为对照组,皮下注射生理盐水;第2组为单纯染Mn(MnCl₂)组,皮下注射生理盐水;第3、4组为预处理(Tau+MnCl₂组和CSA+MnCl₂组),分别皮下注射Tau(100 mg/kg)和CSA(1 mg/kg)。皮下注射2 h后,第1组腹腔注射生理盐水,第2~4组腹腔注射MnCl₂溶液(32 mg/kg),染Mn 30天,Tau和CSA隔日注射1次,共干预15次。最后1次染Mn后24 h,切取肝组织。测定肝线粒体膜肿胀度、膜电位、PT孔和SDH活性、细胞色素C含量以及GSH-PX活性、OH.含量。结果:大鼠单纯染Mn 30天后,与对照组比较线粒体膜肿胀度光密度降低(P<0.05),PT孔、线粒体膜电位光密度降低,GSH-PX和SDH活性降低,细胞色素C和OH.含量升高(P<0.05~P<0.01);Tau+MnCl₂组与MnCl₂组相比,线粒体膜肿胀度光密度、PT孔、线粒体膜电位光密度升高(P<0.05~P<0.01),GSH-PX和SDH活性升高,细胞色素C和OH.含量降低(P<0.01);CSA+MnCl₂组与MnCl₂组相比,PT孔、线粒体膜电位光密度升高,GSH-PX和SDH活性升高,细胞色素C含量降低(P<0.01)。结论:Tau和CSA对Mn引起的肝脏线粒体氧化损伤有不同程度的拮抗作用。

English Abstract

Effect of taurine and cyclosporine A on oxidative damage of liver mitochondrial induced by manganese chloride in rats

Department of Hygiology, Bengbu Medical College, Bengbu Anhui 233030, China

Received Date: 2010-05-10

Abstract: Objective: To study the effect of different doses of manganese (Mn) on oxidative damage of liver mitochondrial induced by Mn chloride,and to explore the cell molecular mechanism of Mn-induced exeitotoxicity.Methods: Twenty four male SD rats were randomly divided into four groups by weight.The first group (control group) were given subcutaneous injection of physiological saline only;the second group (Mn-exposed group) were injected 32 mg/kg of MnCl₂ subcutaneously;the third and fourth groups were intraperitoneally injected 100 mg/kg of taurine (Tau) and 1 mg/kg of cyclosporine A (CSA),respectively.Two hours after subcutaneous injection,the first group were intraperitoneally injected physiological saline,and the other three groups received intraperitoneal injection of 32 mg/kg of MnCl₂ for 30 days,and Tau and CSA were injected every other day for 15 times.At the 24th hour after the last administration of MnCl₂,the rats were killed and the liver was taken to detect the mitochondrial swelling amplitude,mitochondrial membrane potential (MMP),permeability transition pore (PT pore),the activity of GSH-PX,SDH and the content of cytochrome C and OH·.Results: Compared with control group,the mitochondrial swelling amplitude,PT pore,MMP,the activity of GSH-PX and SDH decreased in the MnCl₂ group,while the content of cytochrome C and OH·increased (P<0.05 to P<0.01).Compared with MnCl₂ group,the mitochondrial swelling amplitude,PT pore and MMP increased in Tau pretreatment group (P<0.05 to P<0.01),while the activity of GSH-PX and SDH increased,and the content of cytochrome C and OH·decreased (P<0.01).Compared with control group,the activity of GSH-PX and SDH,PT pore and MMP increased in CSA pretreatment group,while the content of cytochrome C decreased (P<0.01).Conclusions: Tau and CSA have some antagonistic effects on oxidative damage of liver mitochondrial induced by manganese.