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绿原酸对牛肠上皮细胞双氧水氧化损伤的缓解作用。

Alleviating effect of chlorogenic acid on oxidative damage caused by hydrogen peroxide in bovine intestinal epithelial cells.

机构信息

Henan International Joint Laboratory of Animal Welfare and Health Breeding, Henan University of Science and Technology, Luoyang, China.

出版信息

J Vet Med Sci. 2024 Sep 20;86(9):1016-1026. doi: 10.1292/jvms.24-0148. Epub 2024 Jul 29.

DOI:10.1292/jvms.24-0148
PMID:39069486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11422687/
Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/82b35ffab0a5/jvms-86-1016-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/6468e6c9bd80/jvms-86-1016-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/87253758b189/jvms-86-1016-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/626d65e05569/jvms-86-1016-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/fa17bd799647/jvms-86-1016-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/891230d3437d/jvms-86-1016-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/2d143257839b/jvms-86-1016-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/82b35ffab0a5/jvms-86-1016-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/6468e6c9bd80/jvms-86-1016-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/87253758b189/jvms-86-1016-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/626d65e05569/jvms-86-1016-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/fa17bd799647/jvms-86-1016-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/891230d3437d/jvms-86-1016-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/2d143257839b/jvms-86-1016-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c892/11422687/82b35ffab0a5/jvms-86-1016-g007.jpg

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