Authors
Şahhan Kılıç, Süha Asal, Mert Babaoğlu, Cumaali Demirtaş, Samet Yavuz, Eray Metin Güler, Hakan Beyaztaş, Yavuz Aslan, Cansu Türker Sarıçoban, Özge Bengisu Uysal, Mehmet Yıldırım, Mert İlker Hayıroğlu, Tufan Çınar
Published in
Fundamental & clinical pharmacology. Volume 40. Issue 4. Pages e70102.
Abstract
Lower extremity ischemia-reperfusion injury (IRI) triggers systemic inflammation and oxidative stress, causing myocardial remote ischemia-reperfusion injury (MIRI). Current treatments are limited.
Male Sprague-Dawley rats (n = 6 per group) were assigned to Sham, I/R, I/R + colchicine (C), I/R + HBOT, and I/R + HBOT + C. IRI was induced by 60-min infrarenal aortic clamping and 120-h reperfusion.
Once daily colchicine (0.3 mg/kg) and HBOT (2.5 ATA, 100% O2) twice daily were administered for 5 days post-reperfusion. Cardiac damage, oxidative stress, inflammation, and NRF-2/HO-1 signaling were measured, and electrocardiography (ECG) was performed.
I/R caused severe MIRI (Hs-Troponin T: 568.54 pg/mL; heart OSI: 20.98; TNF-α: 582.89 pg/mL). Both monotherapies reduced damage, but HBOT + C was superior: Hs-Troponin T 342.07 pg/mL, OSI 2.26, TNF-α 278.82 pg/mL, and IL-6 12.25 pg/mL, with the upper end of the interquartile range for NRF-2 (41.03) and HO-1 (14.45) activation and restored redox balance (%DIS/NT: 26.31). No differences were observed between groups on the ECG.
Colchicine suppresses inflammation, relieving inhibition of antioxidant defenses, enabling HBOT to fully activate NRF-2/HO-1. This synergistic HBOT + C strategy effectively mitigates MIRI, offering a promising multimodal therapy for remote organ protection after major ischemia.
PMID:
42363694
Bibliographic data and abstract were imported from PubMed on 27 Jun 2026.
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