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Research Snapshot Theater: Resuscitation, Adult and Pediatric and Veterinarian

Hypothermia Attenuates Post-Resuscitation Renal Injury via AMPK/Sirt1/p-NF-κB in a Rat Model of CPR

Monday, March 23, 2026
2:30 PM - 3:30 PM Central Time
Location: Connections Central - RST 17
  • ZH

    Zhanghuan HE, n/a (she/her/hers)

    Beijing, China (People's Republic)

    Disclosure(s): No relevant financial relationship(s) to disclose.

  • Pei Liu, n/a (she/her/hers)

    CHN

    Disclosure(s): No relevant financial relationship(s) to disclose.

  • Lirong Wang, n/a

    China (People's Republic)

    Disclosure(s): No relevant financial relationship(s) to disclose.

  • JH

    Jiawei HE, n/a

    N/A
    Department of Critical Care Medicine, Beijing Friendship Hospital, Capital Medical University, Beijing, China (People's Republic)

    Disclosure information not submitted.

  • SZ

    Shen Zhao, n/a

    Chief Physician
    Department of Critical Care Medicine, Beijing Friendship Hospital, Capital Medical University

    Disclosure information not submitted.

Introduction: Post-resuscitation acute kidney injury (AKI) is a major determinant of mortality after cardiac arrest. We hypothesized that therapeutic hypothermia would attenuate AKI by activating the AMPK/Sirt1/p-NF-κB pathway and thereby suppressing inflammation.


Methods: Twenty-four adult male Sprague-Dawley rats underwent 8 minutes of asphyxial cardiac arrest followed by standardized cardiopulmonary resuscitation. Five minutes after return of spontaneous circulation, animals were randomized to normothermia group (NT, 37 ± 0.5 °C; n = 12), hypothermia group (HT, 33 ± 0.5 °C; n = 12) for 6 hours. Sham-operated rats (n=5) served as controls. Survival was monitored for 24 hours. Serum creatinine, blood urea nitrogen (BUN), neutrophil gelatinase associated lipocalin (NGAL), and cytokines (TNF-α, IL-1β, IL-6) were measured using enzyme-linked immunosorbent assay (ELISA) at baseline and 24 hours post-resuscitation. Renal injury was graded histologically (H&E staining) and expression of phosphorylated AMPK, Sirt1, and NF-κB-p65 in renal cortex at 24 hours post-resuscitation was quantified by Western blot.


Results: Compared with NT,HT group demonstrated increased survival rate (p < 0.05) and improved renal function (creatinine 68.56 ± 12.76 vs. 122.98± 13.83  mg/dL; BUN 11.67 ± 0.96 vs. 18.34 ± 1.31 mg/dL; NGAL 10.71 ± 1.60 vs. 18.56 ± 1.46 ng/mL; all p < 0.01). Compared with NT, a lower histologic injury score was observed in HT group (1.3 ± 0.4 vs 3.2 ± 0.5; p < 0.05). Compared with NT, decreased pro-inflammatory cytokines were observed in HT ( TNF-α 21.42±1.99 vs. 33.24±2.29 pg/ml, IL-1β 45.75±4.72 vs. 75.63±3.94 pg/ml, IL-6 40.75±4.72 vs. 56.63±3.94 pg/ml, all p < 0.01). Compared with NT, phosphorylation of AMPK, Sirt1, and NF-κB p65 were increased 2.8-, 3.9-, and 3.8-fold, respectively, in HT (all p < 0.01).


Conclusions: Early post-resuscitation hypothermia mitigated structural and functional renal injury, suppressed systemic inflammation, and improved short-term survival in this rat CPR model. These benefits appear to be mediated, at least in part, through activation of the AMPK/Sirt1/p-NF-κB axis.