ArticleArchiv der Pharmazie2025
Unveiling the Therapeutic Potential of Dulaglutide in Mitigating Tacrolimus-Induced Nephrotoxicity Through Targeting the miR-22/HMGB-1/TLR4/MyD88/NF-κB Trajectory.
Article in Archiv der Pharmazie, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Glutamine reprogramming affects the tumor microenvironment and immune response in hepatocellular carcinoma.Molecular biology reports · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
Tacrolimus (Tac) is an immunosuppressive drug used to reduce the risk of allograft rejection; however, it can induce renal injury. High mobility group box 1 (HMGB-1) protein, which induces inflammation through the aberrant stimulation of the Toll-like receptor 4 (TLR4)/myeloid differentiation primary response protein (MyD88)/nuclear factor kappa B (NF-κB) trajectory, could represent a molecular target for alleviating Tac-induced renal damage. The present study aimed to investigate the potential protective role of the GLP-1 agonist, dulaglutide (Dula), against Tac-induced nephrotoxicity in rats. Rats were administered Tac (5 mg/kg/day) and vehicle or Dula (0.2 mg/kg once a week) for 14 days. Treatment with Dula reduced serum creatinine plus blood urea nitrogen and attenuated Tac-induced renal histopathological changes. Dula treatment also hampered renal inflammation and restored redox homeostasis, as indicated by remarkably reduced tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), malondialdehyde (MDA), and NADPH oxidase 1 levels alongside marked replenishment in reduced glutathione (GSH) content. These effects were mediated through the upregulation of miR-22 expression and the consequent inhibition of the HMGB-1/TLR4/MyD88/NF-κB trajectory. Collectively, Dula has been demonstrated to protect rats against Tac-induced nephrotoxicity by reducing inflammation, restoring redox homeostasis, and modulation of the miR-22/HMGB-1/TLR4/MyD88/NF-κB trajectory. Dula may be beneficial clinically in preventing Tac-induced renal injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.