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RESEARCH ARTICLE

Amlodipine Protects against Methotrexate-Induced Acute Kidney Injury in Rats

Dina Kutbi1 , 2 , * Open Modal Authors Info & Affiliations
The Open Biochemistry Journal 20 May 2024 RESEARCH ARTICLE DOI: 10.2174/011874091X312641240424110832

Abstract

Background

Methotrexate (MTX) is a commonly used chemotherapy drug with known nephrotoxic effects, including the potential for acute kidney injury. However, the precise mechanism through which MTX induces nephrotoxicity remains unclear, though oxidative stress and direct toxic effects on renal tubules are believed to play key roles. Recent studies suggest that calcium channel blockers may offer promise in slowing down the progression of chronic kidney diseases.

Objective

The purpose of this study was to explore the potential of Amlodipine, a calcium channel blocker, to alleviate acute kidney injury caused by the administration of MTX in rats.

Methods

Three groups of twenty-four male Wistar rats were randomly assigned: Group 1—the control group was given normal saline orally. Group II, underwent five days of continuous administration of a single intraperitoneal (IP) dosage of 20 mg/kg MTX. The same dosage of MTX was given to Group III followed by an oral dose of Amlodipine at 5 mg/kg over the same period. Upon completion of the experiment, serum biochemical parameters, renal damage markers, oxidative stress, inflammatory markers, and kidney tissue histology were assessed.

Results

The results indicate that MTX administration significantly increased the levels of serum biochemical parameters, renal damage markers, inflammatory markers, oxidative stress markers, and induced alterations in kidney histology. However, the administration of Amlodipine following MTX treatment protected against these changes.

Conclusion

Amlodipine exhibits therapeutic potential in mitigating MTX-induced kidney injury in rats and its associated side effects.

Keywords: Amlodipine, Kidney injury, Methotrexate, Nephrotoxicity, Renoprotection, Oxidative stress, Inflammation.
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