Henan International Joint Laboratory of Animal Welfare and Health Breeding, Henan University of Science and Technology, Luoyang, China.
J Vet Med Sci. 2024 Sep 20;86(9):1016-1026. doi: 10.1292/jvms.24-0148. Epub 2024 Jul 29.
Chlorogenic acid (CGA) is a polyphenol substance contained in many plants, which has good antioxidant activity. This experiment aimed to explore the protective effects of CGA on hydrogen peroxide (HO)-induced inflammatory response, apoptosis, and antioxidant capacity of bovine intestinal epithelial cells (BIECs-21) under oxidative stress and its mechanism. The results showed that compared with cells treated with HO alone, CGA pretreatment could improve the viability of BIECs-21. Importantly, Chlorogenic acid pretreatment significantly reduced the formation of malondialdehyde (MDA), lowered reactive oxygen species (ROS) levels, and enhanced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) (P<0.05). In addition, CGA can also improve the intestinal barrier by increasing the abundance of tight junction proteins claudin-1 and occludin. Meanwhile, CGA can reduce the gene expression levels of pro-inflammatory factors Interleukin-6 (IL-6) and Interleukin-8 (IL-8), increase the expression of anti-inflammatory factor Interleukin-10 (IL-10), promote the expression of the nuclear factor-related factor 2 (Nrf2) signaling pathway, enhance cell antioxidant capacity, and inhibit Nuclear Factor Kappa B (NF-κB) the activation of the signaling pathway reducing the inflammatory response, thereby alleviating inflammation and oxidative stress damage.
绿原酸(CGA)是许多植物中含有的多酚物质,具有良好的抗氧化活性。本实验旨在探讨 CGA 在氧化应激下对双氧水(HO)诱导的牛肠上皮细胞(BIECs-21)炎症反应、细胞凋亡和抗氧化能力的保护作用及其机制。结果表明,与单独用 HO 处理的细胞相比,CGA 预处理能提高 BIECs-21 的活力。重要的是,绿原酸预处理能显著降低丙二醛(MDA)的形成,降低活性氧(ROS)水平,并增强超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-PX)的活性(P<0.05)。此外,CGA 还可以通过增加紧密连接蛋白 Claudin-1 和 Occludin 的丰度来改善肠道屏障。同时,CGA 可以降低促炎因子白细胞介素-6(IL-6)和白细胞介素-8(IL-8)的基因表达水平,增加抗炎因子白细胞介素-10(IL-10)的表达,促进核因子相关因子 2(Nrf2)信号通路的表达,增强细胞抗氧化能力,抑制核因子 Kappa B(NF-κB)信号通路的激活,从而减轻炎症反应,缓解炎症和氧化应激损伤。