酸对牛肠表皮细胞中过氧化引起的氧化损伤具有缓解作用
Jia Lu1, Yongsheng An1, Xueying Wang1
1Henan International Joint Laboratory of Animal Welfare and Health Breeding, Henan University of Science and Technology, Luoyang, China.
The Journal of veterinary medical science
|July 28, 2024
概括
酸 (CGA) 通过减少炎症和提高抗氧化能力来保护牛肠道细胞免受氧化应激. CGA增强了细胞活力,加强了肠道屏障,证明了它的治疗潜力.
科学领域:
- * 细胞生物学 * 细胞生物学
- * 生物化学 * 生物化学
- * 药理学 药理学 药理学
背景情况:
- *氧化应激会损害肠道上皮细胞,导致炎症和亡.
- * 基酸 (CGA) 是一种植物多,具有抗氧化特性.
- * 牛肠上皮细胞 (BIECs-21) 容易受到过氧化 (H2O2) 引起的损伤.
研究的目的:
- * 在BIECs-21中研究CGA对H2O2引起的氧化应激的保护作用.
- *阐明涉及炎症反应,亡和抗氧化能力的潜在机制.
- * 评估CGA对肠道屏障功能和关键信号通路的影响.
主要方法:
- *BIECs-21在暴露于H2O2之前被CGA预处理.
- *测量了细胞活力,马隆迪化物 (MDA),活性氧物种 (ROS),超氧化物脱氧酶 (SOD) 和谷氨过氧酶 (GSH-PX) 的水平.
- *分析了紧结蛋白 (克劳丁-1,奥克卢丁),炎性细胞因子 (IL-6,IL-8,IL-10) 和信号通路 (Nrf2,NF-κB) 的表达.
主要成果:
- *CGA预处理显著改善了BIECs-21的生存能力,而不是单独使用H2O2.
- *CGA降低了MDA和ROS水平,同时增强了SOD和GSH-PX活动 (P<0.05).
- *CGA增加了紧结蛋白,调节炎性细胞因子 (减少IL-6/IL-8,增加IL-10),激活了Nrf2,并抑制了NF-κB.
结论:
- *CGA在牛肠细胞中显示出对H2O2诱导的氧化应激具有显著的保护作用.
- *CGA增强抗氧化能力,改善肠道屏障功能,调节炎症信号通路.
- *CGA显示出作为减轻肠道炎症和氧化损伤的治疗剂的潜力.
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