Liu · Journal of thermal biology 2025 · Controlled animal and in vitro laboratory experiment · n=?

Intermittent mild cold stimulation ameliorates hypothermic damage to broiler pectoral muscle by modulating the Nrf2/Keap1/AREs and AMPK/PGC-1α signaling pathways.

Cited 2 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Bench and animal research without human subjects (Oxford Level 5).

PubMed 40953554 · doi:10.1016/j.jtherbio.2025.104254 · record verified 2026-08-30

What was done

Broilers were divided into a control group (CC) and two cold-exposure groups (C3 and C9). In parallel, broiler-derived myoblasts were cultured under control (C37) or cold-exposure conditions (C32 and C27). The researchers evaluated meat quality parameters (lightness L*, redness a*, yellowness b*, and drip loss), heat shock protein (HSP) expression, apoptotic markers (Bcl-2/Bax ratio, cytochrome c, Caspase-3, Caspase-8, and Caspase-9), antioxidant enzymes (CAT, GPx, SOD2), and key metabolic signaling regulators (Nrf2/Keap1/AREs and AMPK/PGC-1α).

What was found

The abstract reports directional changes without numeric values or effect sizes. In broilers, the C9 group had lower L* and a* values compared with CC and C3, along with higher b* values and increased drip loss compared with C3. HSP mRNA and protein levels were significantly higher in C9 than CC. Apoptotic markers (CytC, Caspase-3, Caspase-8, Caspase-9) were elevated in cold-exposed broilers, and the Bcl-2/Bax ratio was significantly reduced in the C9 group. Catalase (CAT) levels increased and the Nrf2 pathway was activated in the C3 group but not in the C9 group. AMPK and PGC-1α levels increased following cold stimulation. In vitro, C32 and C27 reduced HSP60 and HSP70 compared to C37 while increasing apoptotic proteins; AMPK and PGC-1α were significantly increased at C32 but decreased at C27.

Why it matters

The study identifies differential molecular responses between mild and severe cold exposure in poultry, showing that mild cold engages adaptive antioxidant and metabolic pathways (Nrf2 and AMPK/PGC-1α) that may protect against hypothermic muscle damage.

Limits

This is purely an animal and cell-culture study with no clinical application to humans. The abstract omits sample sizes for both the broiler cohorts and cell culture replicates, does not define the exact experimental parameters for in vivo groups (such as temperature or duration for C3 and C9), and provides no quantitative data, error margins, or exact p-values.

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