- VernacularTitle:枸橼酸镁对慢性肾衰竭环境下氧化应激的抑制作用
- Author:
Zhihui YAO
1
;
Weidong MA
1
;
Tuo HAN
1
;
Yajie FAN
1
;
Chunyan ZHANG
1
;
Yan ZHANG
1
;
Yanchao HU
1
;
Congxia WANG
1
Author Information
- Publication Type:Journal Article
- Keywords: magnesium citrate (MgCit); chronic renal failure (CRF); rat; uremia; vascular smooth muscle cell (VSMCs); oxidative stress
- From: Journal of Xi'an Jiaotong University(Medical Sciences) 2024;45(5):712-717
- CountryChina
- Language:Chinese
- Abstract: 【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.