ArticleRenal failure2024
Mechanism of dexmedetomidine protection against cisplatin induced acute kidney injury in rats.
Article in Renal failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Renoprotective effects of perampanel against cisplatin-induced acute kidney injury: managing NLRP3-pyroptosis and enhancement of antioxidant defense.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Pyroptosis-induced tissue damage in kidney disease.Renal failure · 2025Review
- Rescue RM/CS-AKI by blocking strategy with one-dose anti-myoglobin RabMAb.Nature communications · 2025Article
- The protective effects of the combination ofOpen veterinary journal · 2025Article
- The regulatory role of dexmedetomidine in NLRP3 inflammasome-related organ protection.Journal of anesthesia and translational medicine · 2024Review
- ALKBH5 insufficiency protects against ferroptosis-driven cisplatin-induced renal cytotoxicity.Cell biology and toxicology · 2024Article
- The effectiveness of dexmedetomidine for preventing acute kidney injury after surgery: a systematic review and meta-analysis.Frontiers in medicine · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study explored the molecular mechanisms by which dexmedetomidine (Dex) alleviates cisplatin (CP)-induced acute kidney injury (AKI) in rats.
methodsCP-induced AKI models were established, and Dex was intraperitoneally injected at different concentrations into rats in the model groups. Subsequently, rats were assigned to the control, CP, CP + Dex 10 μg/kg, and CP + Dex 25 μg/kg groups. After weighing the kidneys of the rats, the kidney arterial resistive index was calculated, and CP-induced AKI was evaluated. In addition, four serum biochemical indices were measured: histopathological damage in rat kidneys was detected; levels of inflammatory factors, interleukin (IL)-1β, IL-18, IL-6, and tumor necrosis factor alpha, in kidney tissue homogenate of rats were assessed through enzyme-linked immunosorbent assay (ELISA); and levels of NLRP-3, caspase-1, cleaved caspase-1, gasdermin D (GSDMD), and GSDMD-N in kidney tissues of rats were determined
resultsDex treatment reduced nephromegaly and serum clinical marker upregulation caused by CP-induced AKI. In addition, hematoxylin and eosin staining revealed that Dex treatment relieved CP-induced kidney tissue injury in AKI rats. ELISA analyses demonstrated that Dex treatment reduced the upregulated levels of proinflammatory cytokines in the kidney tissue of AKI rats induced by CP, thereby alleviating kidney tissue injury. Western blotting indicated that Dex alleviated CP-induced AKI by inhibiting pyroptosis mediated by NLRP-3 and caspase-1.
conclusionDex protected rats from CP-induced AKI, and the mechanism may be related to NLRP-3/Caspase-1-mediated pyroptosis.
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