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姜黄素通过 NFE2L2 信号通路减轻 LPS 诱导的奶牛乳腺上皮细胞氧化应激、炎症和细胞凋亡。

Curcumin Alleviates LPS-Induced Oxidative Stress, Inflammation and Apoptosis in Bovine Mammary Epithelial Cells via the NFE2L2 Signaling Pathway.

机构信息

Key Laboratory of Zoonosis Research, Ministry of Education, Department of Animal Science, College of Animal Sciences, Jilin University, Changchun 130062, China.

出版信息

Toxins (Basel). 2021 Mar 12;13(3):208. doi: 10.3390/toxins13030208.

DOI:10.3390/toxins13030208
PMID:33809242
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7999830/
Abstract

Lipopolysaccharide (LPS) is an endotoxin, which may cause immune response and inflammation of bovine mammary glands. Mastitis impairs animal health and results in economic loss. Curcumin (CUR) is a naturally occurring diketone compound, which has attracted widespread attention as a potential anti-inflammatory antioxidant. The purpose of this study is to investigate whether CUR can reduce the damage of bovine mammary epithelial cells (MAC-T) induced by LPS and its underlying molecular mechanism. The MAC-T cell line was treated with different concentrations of LPS and CUR for 24 h. The results showed that CUR rescued the decrease of MAC-T cell viability and cell damage induced by LPS. At the same time, 10 µM CUR and 100 µg/mL LPS were used to treat the cells in the follow-up study. The results showed CUR treatment reduced the accumulation of reactive oxygen species (ROS), the expression of inflammatory cytokines (tumor necrosis factor-a (TNF-α), interleukin-8 (IL-8), IL-6 and IL-1β) and the rate of apoptosis induced by LPS. These effects were associated with the activation of the nuclear factor E2-related factor 2 (NFE2L2)-antioxidant response element (ARE) pathway coupled with inactivation of the nuclear factor-κB (NF-κB) inflammatory and caspase/Bcl2 apoptotic pathways.

摘要

脂多糖(LPS)是一种内毒素,可能引起牛乳腺的免疫反应和炎症。乳腺炎会损害动物健康并导致经济损失。姜黄素(CUR)是一种天然存在的二酮化合物,作为一种潜在的抗炎抗氧化剂,已引起广泛关注。本研究旨在探讨 CUR 是否可以减轻 LPS 诱导的奶牛乳腺上皮细胞(MAC-T)损伤及其潜在的分子机制。MAC-T 细胞系用不同浓度的 LPS 和 CUR 处理 24 小时。结果表明,CUR 挽救了 LPS 诱导的 MAC-T 细胞活力和细胞损伤的下降。同时,在后续研究中使用 10 μM CUR 和 100 μg/mL LPS 处理细胞。结果表明,CUR 处理减少了 LPS 诱导的活性氧(ROS)积累、炎症细胞因子(肿瘤坏死因子-α(TNF-α)、白细胞介素-8(IL-8)、IL-6 和 IL-1β)的表达和细胞凋亡率。这些作用与核因子 E2 相关因子 2(NFE2L2)-抗氧化反应元件(ARE)通路的激活有关,同时伴有核因子-κB(NF-κB)炎症和 caspase/Bcl2 凋亡通路的失活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/15a0/7999830/d325abf71595/toxins-13-00208-g007.jpg
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