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Updated: Aug 5, 2026

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
Chlorogenic acid supplementation regulates redox status, hepatic inflammation, and mitochondrial function in weaned
1School of Biological Engineering, Henan University of Technology, Zhengzhou 450001, China Correspondence to: K. Cheng,
Abstract:
This study was designed to investigate the effect of chlorogenic acid (CGA) on redox status, hepatic inflammation, and mitochondrial function in weaned piglets with intrauterine growth retardation (IUGR). In total, 24 IUGR male piglets (1.59±0.11 kg) and 24 same-sex normal birth weight (NBW) littermates (0.94±0.06 kg) were selected at birth. After weaning at 26 days of age, NBW and IUGR piglets were fed either a basal diet or a CGA-supplemented diet for 21 days. Thus, all piglets were distributed into groups of 4 treatments × 6 replicates × 2 piglets per replicate. The IUGR piglets showed 18.05%, 28.59%, 23.78%, 27.17%, and 18.61% lower hepatic absolute weight, total superoxide dismutase (T-SOD) activity, GSH, ATP, and complex I levels, and 103.77% and 61.32% higher interleukin 1 beta (IL1β) content and IL18 mRNA expression, respectively, than the NBW piglets. Serum MDA concentration was 34.76% higher and glutathione peroxidase (GPX) activity was 24.18% lower in the IUGR piglets than in the NBW piglets. CGA supplementation decreased serum alanine aminotransferase activity by 29.44%, increased hepatic T-SOD activity by 24.43%, and upregulated complex I concentration by 21.76%. CGA supplementation reversed the IUGR-induced decreases in the activities of serum T-SOD and GPX and hepatic ATP level, increased hepatic IL1β level and IL18 mRNA expression in piglets. A diet supplemented with CGA reduced hepatic MDA content in the IUGR piglets. The results indicate that CGA may improve redox status, inflammation, and mitochondrial function, ultimately alleviating hepatic injury in IUGR piglets.
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