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Anti-oxidative effect of AST-120 on kidney injury after myocardial infarction
Hideki Fujii1, Yuriko Yonekura1, Yusuke Yamashita2
1Division of Nephrology and Kidney Center, Kobe University Graduate School of Medicine, Kobe, Japan.
Insights
AST-120 reduced kidney injury and oxidative stress in rats with myocardial infarction. This treatment lowered indoxyl sulfate levels, suggesting a protective effect against kidney damage post-heart attack.
Area of Science:
- Nephrology
- Cardiology
- Toxicology
Background:
- Chronic kidney disease (CKD) significantly elevates cardiovascular disease (CVD) risk.
- Combined CKD and CVD lead to increased morbidity and mortality.
- Myocardial infarction (MI) is a major cardiovascular event.
Purpose of the Study:
- Investigate the effects of AST-120 on oxidative stress.
- Assess AST-120's impact on kidney injury in a rat model of MI.
- Evaluate AST-120's role in managing uremic toxins like indoxyl sulfate (IS).
Main Methods:
- Male spontaneously hypertensive rats (SHR) underwent MI and were divided into MI and MI+AST-120 groups.
- AST-120 treatment commenced post-MI.
- Analyses included blood/urine tests, mRNA expression, renal histology, and echocardiography.
Main Results:
- AST-120 treatment reduced elevated serum and urine indoxyl sulfate (IS) levels.
- Markers of oxidative stress and kidney injury were decreased in the AST-120 group.
- Renal expression of kidney injury markers and intrarenal oxidative stress were reduced by AST-120.
Conclusions:
- Serum IS levels increased following MI.
- AST-120 demonstrated protective effects against kidney injury post-MI.
- AST-120 may exert its protective effects by suppressing oxidative stress.
Background And Purpose:
Chronic kidney disease (CKD) is a crucial risk factor for cardiovascular disease (CVD), and combined CKD and CVD further increases morbidity and mortality. Here, we investigated effects of AST-120 on oxidative stress and kidney injury using a model of myocardial infarction (MI) in rats.
Experimental Approach:
At 10 weeks, male spontaneously hypertensive rats (SHR) were divided into three groups: SHR (n = 6), MI (n = 8) and MI + AST-120 (n = 8). AST-120 administration was started at 11 weeks after MI. At 18 weeks, the rats were killed, and blood and urine, mRNA expression and renal histological analyses were performed. Echocardiography was performed before and after MI.
Key Results:
At 18 weeks, the BP was significantly lower in the MI and MI+AST-120 groups than in the SHR group. Elevated levels of indoxyl sulfate (IS), one of the uremic toxins, in serum and urine were reduced by AST-120 treatment, compared with the MI group. Markers of oxidative stress in urine and serum biomarkers of kidney injury were decreased in the MI+AST-120 group compared with the other two groups. Renal expression of mRNAs for kidney injury related-markers were decreased in the MI+AST-120 group, compared with the MI group. In vitro data also supported the influence of IS on kidney injury. Immunohistological analysis showed that intrarenal oxidative stress was reduced by AST-120 administration.
Conclusions And Implications:
Serum IS was increased after MI and treatment with AST-120 may have protective effects on kidney injury after MI by suppressing oxidative stress.
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