Dipicolinic acid has an anti-inflammatory effect and inhibits the expression of NF-κB, miR-101a, miR-140 and miR-195 in diclofenac-induced myocardial injury in rats.

Authors

E D Kryl'skii, T N Popova, A N Verevkin, O A Scherbakova, V P Sergin

Published in

Molecular biology reports. Volume 53. Issue 1. Oct 25, 2026. Epub Oct 25, 2026.

Abstract

Nonsteroidal anti-inflammatory drugs, including diclofenac, are commonly used to alleviate inflammation and pain associated with various medical conditions. Prolonged use of these medications may lead to complications related to the cardiovascular system. One of the primary mechanisms of myocardial damage associated with diclofenac is oxidative stress, which is closely linked with the activation of inflammation. The current study aims to evaluate the efficacy of dipicolinic acid (DPA) as a potential treatment for diclofenac-induced cardiac injury. Additionally, the study will investigate the effects of DPA on the expression levels of transcription factor NF-κB and microRNAs (miRNAs), specifically miR-101a, miR-140, and miR-195, which play a role in regulating inflammation.
The results of the study demonstrated that the implementation of DPA led to a substantial reduction in the levels of cardiomyocytes cytolytic markers in the blood serum of the animals, compared to the values observed in the group with myocardial injury. These alterations were associated with decreased concentrations of free radical-induced oxidation products of lipid, protein, and DNA, including diene conjugates, carbonylated proteins, and 8-hydroxy-2-deoxyguanosine. The improvement in the oxidative status of rats was accompanied by a reduction in the levels of pro-inflammatory cytokine mRNA and myeloperoxidase activity. The DPA treatment also reduced the expression of the p65 subunit of the NF-κB factor and miR-101a, miR-140, and miR-195, which were found to be involved in pro-inflammatory signaling.
Therefore, the administration of DPA in diclofenac-induced myocardial injury is associated with an improvement in oxidative status and the inhibition of the inflammatory response, which may involve the modulation of the NF-κB, miR-101, miR-140, and miR-195 expression.

PMID:
42927574
Bibliographic data and abstract were imported from PubMed on 26 Oct 2026.

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