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Published on: December 22, 2023
Magnesium Citrate Protects Against Vascular Calcification in an Adenine-induced Chronic Renal Failure Rat Model
Zhihui Yao1, Yang Xu1, Weidong Ma1
1Department of Cardiovascular Medicine, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Insights
Magnesium citrate (MgCit) helps prevent vascular calcification (VC) in rats with chronic renal failure (CRF). This study suggests MgCit may be a potential therapeutic for preventing VC in CRF patients.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Biochemistry
Background:
- Hypomagnesemia is a significant risk factor for cardiovascular disease in chronic renal failure (CRF) patients.
- The precise impact of magnesium (Mg) on vascular calcification (VC) in CRF remains unclear.
Purpose of the Study:
- To investigate the protective effects of magnesium citrate (MgCit) against vascular calcification (VC) in a rat model of chronic renal failure (CRF).
Main Methods:
- Rats with CRF were induced using adenine and phosphorus, then treated with varying doses of MgCit.
- Evaluated VC markers including calcium and phosphorus content, alkaline phosphatase activity, and expression of alpha smooth muscle actin and RUNX2 in aortic tissues.
Main Results:
- The CRF model group exhibited significant VC.
- MgCit treatment dose-dependently reduced VC, decreasing calcium and phosphorus levels, alkaline phosphatase activity, and RUNX2 expression, while increasing alpha smooth muscle actin.
Conclusions:
- Magnesium citrate (MgCit) demonstrates a protective effect against vascular calcification (VC) in rats with chronic renal failure (CRF).
- MgCit shows potential as a therapeutic agent for preventing VC in patients suffering from CRF.
Background:
Hypomagnesemia was identified as a strong risk factor for cardiovascular disease in patients with chronic renal failure (CRF). However, the effects of magnesium (Mg) on vascular calcification (VC) have not been fully elucidated. Thus, we aim to determine the effects of Mg citrate (MgCit) on VC in CRF rats.
Methods:
Rats were divided into 5 groups: group 1 (normal diet), group 2 (normal diet with MgCit), group 3 (the VC model of CRF induced by 0.75% adenine and 0.9% phosphorus diet from day 1 to day 28), group 4 (group 3 treated with low-dose MgCit from day 1 to day 42), and group 5 (same as group 3 except the high-dose MgCit). All rats were killed at day 43 with collection of blood and aortas. Then, serum biochemical parameters, VC-related staining, calcium and P contents, alkaline phosphatase contents and activity, expression of alpha smooth muscle actin, and runt-related transcription factor 2 (RUNX2) in aortas were assessed.
Results:
Group 3 had extensive VC. The VC degree decreased in groups 4 and 5 in a dose-depended manner with reduced calcium content, P levels, alkaline phosphatase content and activity, and protein levels of RUNX2 and increased protein levels of alpha smooth muscle actin in aortas.
Conclusions:
MgCit exerted a protective role in VC in adenine-induced CRF rats; thus, it may be a potential drug for the prevention of VC in patients with CRF.
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