Huang Qi, Shan Qiang, Ma Fengtao, Li Shengli, Sun Peng
State Key Laboratory of Animal Nutrition and Feeding, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
State Key Laboratory of Animal Nutrition and Feeding, Beijing Engineering Technology Research Center of Raw Milk Quality and Safety Control, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China.
Int J Biol Macromol. 2025 Apr;301:140133. doi: 10.1016/j.ijbiomac.2025.140133. Epub 2025 Jan 21.
Chlorogenic acid (CGA), a polyphenolic bioactive molecule derived from medicinal plants, is known for its strong antioxidant and anti-inflammatory properties. Previous studies have demonstrated that dietary supplementation with Lonicera japonica extract, rich in CGA, effectively enhances the production performance of lactating dairy cows under heat stress (HS) conditions. However, the molecular mechanisms underlying CGA's protective effects remain unclear. This study aims to elucidate the mechanisms by which CGA alleviates HS-induced oxidative damage in bovine mammary epithelial cells (bMECs), focusing on its pharmacological activity and potential application as a natural therapeutic agent for bovine mammary disorders. The results demonstrated that HS activates the NF-κB and NLRP3 signaling pathways by increasing ROS generation, leading to oxidative stress and inflammatory response in bMECs. CGA mitigates these effects by scavenging intracellular ROS, activating the Nrf2 signaling pathway, and inhibiting key molecules in the NF-κB and NLRP3 signaling pathways. This study provides new insights into the underlying molecular mechanisms of CGA's protective effects, highlighting its potential as a natural antioxidant for bovine mammary health and contributing to the broader application of polyphenolic compounds in managing oxidative stress and inflammation.
绿原酸（CGA）是一种源自药用植物的多酚类生物活性分子，以其强大的抗氧化和抗炎特性而闻名。先前的研究表明，日粮中添加富含CGA的忍冬提取物可有效提高热应激（HS）条件下泌乳奶牛的生产性能。然而，CGA保护作用的分子机制仍不清楚。本研究旨在阐明CGA减轻HS诱导的牛乳腺上皮细胞（bMECs）氧化损伤的机制，重点关注其药理活性以及作为牛乳腺疾病天然治疗剂的潜在应用。结果表明，HS通过增加活性氧（ROS）的产生激活NF-κB和NLRP3信号通路，导致bMECs发生氧化应激和炎症反应。CGA通过清除细胞内ROS、激活Nrf2信号通路以及抑制NF-κB和NLRP3信号通路中的关键分子来减轻这些影响。本研究为CGA保护作用的潜在分子机制提供了新的见解，突出了其作为牛乳腺健康天然抗氧化剂的潜力，并有助于多酚类化合物在管理氧化应激和炎症方面的更广泛应用。
