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Updated: Jan 16, 2026

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Mitigating effects of resveratrol on cold exposed-induced cardiac mitochondrial dysfunction and lipid metabolic
Haidong Wei1, Deyang Miao1, Haochen Li1
1College of Life Science, Northeast Agricultural University, Harbin, China.
Abstract:
Cold climate is a severe challenge to the sustainability of global poultry production, as it impairs the health and growth performance. Resveratrol (RES) is a natural polyphenol and has antioxidative and anti-inflammatory activities. To investigate whether RES alleviates cardiac substance metabolism disorder caused by cold exposure (CE) via regulating mitochondrial quality control. 28-day-old broilers were subjected to CE at 8 ± 1°C for 14 days and fed the diets with 0, 250, 500, and 750 mg RES/kg feed, respectively. CE reduced body weight, and caused mitochondrial structure abnormalities and lipid droplet formation in the heart. CE elevated reactive oxygen species level, reduced mRNA and protein expression of AMPK and genes related to antioxidative function (Nrf2, HO-1, SOD1, SOD2, CAT, and GPx), mitochondrial biogenesis (Nrf1 and PGC-1α), mitochondrial dynamics (MFF, MFN1, MFN2, and OPA1), and lipolysis (PPARα, CPT1, and ACO2), promoted mRNA and protein expression of dynamin-related protein 1 and genes associated with mitophagy (PINK1, Parkin, ATG5, LC3Ⅱ/Ⅰ, p62, and Beclin1) and lipogenesis (SREBP1, FAS, ACC, and PPARγ), increased the concentrations of triglyceride, total cholesterol and LDLC, and reduced free fatty acids and HDLC concentrations in serum. RES reduced CE-caused oxidative stress and improved mitochondrial health, improving lipid metabolism by regulating the AMPK/PGC-1α/PPAR pathway in broiler heart. Therefore, this study suggests that dietary supplementation with RES, especially a 500 mg/kg dosage, could relieve CE-induced heart injury and dysfunction associated with lipid metabolism disorder by improving the Nrf2/HO-1 pathway-modulated antioxidative defense function and balancing the AMPK signaling-regulated mitochondrial quality control system in broilers.
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