枸橼酸镁对慢性肾衰竭环境下氧化应激的抑制作用  

Inhibitory effects of magnesium citrate on oxidative stress in chronic renal failure

作　　者：姚智会 马维冬 韩拓 范雅洁 张春艳[1] 张岩[1] 胡艳超[1] 王聪霞[1] YAO Zhihui;MA Weidong;HAN Tuo;FAN Yajie;ZHANG Chunyan;ZHANG Yan;HU Yanchao;WANG Congxia(Department of Cardiology,The Second Affiliated Hospital of Xi’an Jiaotong University,Xi’an 710004,China)

机构地区：[1]西安交通大学第二附属医院心血管病院,陕西西安710004

出　　处：《西安交通大学学报（医学版）》2024年第5期712-717,共6页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：国家自然科学基金资助项目(No.81273878);陕西省自然科学基础研究计划项目(No.2021JQ-409)。

摘　　要：目的探讨枸橼酸镁(magnesium citrate,MgCit)抑制慢性肾衰竭(chronic renal failure,CRF)环境下氧化应激的作用。方法SD大鼠分为CRF模型组、MgCit组(375、750 mg/kg),另设正常对照组、MgCit对照组(750 mg/kg);透射电镜观察大鼠胸大动脉血管平滑肌细胞(vascular smooth muscle cells,VSMCs)中线粒体形态;利用试剂盒检测大鼠主动脉和血浆中超氧化物歧化酶(superoxide dismutase,SOD)和丙二醛(malonaldehyde,MDA)的含量。培养VSMCs并分为正常对照组、CRF模型组、MgCit组(1.5、3 mmol/L),流式细胞仪定量检测细胞超氧化物阴离子(dihydroethidium,DHE)和细胞凋亡情况。结果与对照组相比,模型组大鼠胸大动脉VSMCs线粒体肿胀,嵴断裂或消失;MgCit干预能减轻线粒体肿胀,未见嵴断裂;模型组大鼠主动脉和血浆SOD水平降低(P<0.05),MDA水平升高(P<0.05);MgCit干预能增加主动脉和血浆SOD水平,并降低MDA水平(P<0.05)。CRF环境下即CRF模型组VSMCs的DHE含量升高,凋亡增加(P<0.05);MgCit干预能降低DHE含量,并抑制凋亡(P<0.05)。结论MgCit抑制CRF大鼠和VSMCs的氧化应激水平。Objective To investigate the inhibitory effects of magnesium citrate(MgCit)on oxidative stress in chronic renal failure(CRF).Methods SD rats were divided into CRF model group,MgCit groups(375 and 750 mg/kg),normal control group,and MgCit control group(750 mg/kg).The morphology of mitochondria in thoracic artery vascular smooth muscle cells(VSMCs)was observed by transmission electron microscopy.The content of superoxide dismutase(SOD)and malonaldehyde(MDA)in rat aorta and plasma was detected by the kit.The VSMCs were divided into normal control group,CRF model group,and MgCit groups(1.5 and 3 mmol/L).The levels of superoxide anion(DHE)and apoptosis were quantitatively detected by flow cytometry.Results Compared with the control groups,the mitochondria were swollen and the cristae fractured or disappeared in the model group;MgCit intervention could reduce mitochondrial swelling,but not cristae fracture.In the model group,SOD level in aorta and plasma decreased(P<0.05)while MDA level increased(P<0.05).MgCit intervention could increase SOD in aorta and plasma,but decrease MDA level(P<0.05).In the CRF environment,the DHE content of VSMCs and apoptosis in CRF model group increased(P<0.05).MgCit intervention could decrease DHE content and inhibit apoptosis(P<0.05).Conclusion MgCit inhibits oxidative stress levels in vivo and in vitro in CRF.

关 键 词：枸橼酸镁(MgCit) 慢性肾衰竭(CRF) 大鼠 尿毒症 血管平滑肌细胞(VSMCs) 氧化应激 

分 类 号：R692.5[医药卫生—泌尿科学]