Key Laboratory of Traditional Chinese Veterinary Medicine and Animal Health in Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, PR China.
Fujian Key Laboratory of Chinese Traditional and Western Veterinary Medicine and Animal Health, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, PR China.
Int J Biol Macromol. 2024 Nov;279(Pt 3):134815. doi: 10.1016/j.ijbiomac.2024.134815. Epub 2024 Aug 21.
Oxidative stress plays an important role in various diseases. miR-221 has been reported to regulate oxidative stress. However, the mechanism of miR-221 in regulating oxidative stress induced by sCPPS remains unclear. This study aimed to investigate the protective effects and mechanisms of miR-221 on oxidative stress induced by sCPPS. The expression of SOD, CAT, MDA, LDH, MMP, caspase-3 activity and apoptosis were measured. In addition, the key signaling factors in the Keap1-Nrf2-ARE signaling pathway were determined by real-time PCR and Western blot. Mice were employed to evaluate the effects of sCPPS and the possible mechanism in vivo. sCPPS promoted the expression of SOD and CAT and activated Keap1-Nrf2-ARE signaling pathway inhibit the MDA content, MMP, caspase-3 activity, apoptosis and LDH release rate after transfection with miR-221 mimics and inhibitors. Consistently, sCPPS has the potential to enhance the expression of antioxidant enzymes as well as upregulate mRNA expression of crucial signal proteins in vivo. miR-221 on oxidative stress protection induced by sCPPS possibly through regulating the Keap1-Nrf2-ARE signaling pathway in macrophages.
氧化应激在各种疾病中起着重要作用。miR-221 已被报道可调节氧化应激。然而，miR-221 调节 sCPPS 诱导的氧化应激的机制尚不清楚。本研究旨在探讨 miR-221 对 sCPPS 诱导的氧化应激的保护作用及其机制。测定 SOD、CAT、MDA、LDH、MMP、caspase-3 活性和细胞凋亡。此外，通过实时 PCR 和 Western blot 测定 Keap1-Nrf2-ARE 信号通路中的关键信号因子。采用小鼠评估 sCPPS 及其在体内的可能机制的影响。sCPPS 促进 SOD 和 CAT 的表达，并激活 Keap1-Nrf2-ARE 信号通路抑制 MDA 含量、MMP、caspase-3 活性、细胞凋亡和 LDH 释放率转染 miR-221 模拟物和抑制剂后。一致地，sCPPS 具有增强抗氧化酶表达的潜力，并且在体内上调关键信号蛋白的 mRNA 表达。miR-221 对 sCPPS 诱导的氧化应激的保护作用可能是通过调节巨噬细胞中的 Keap1-Nrf2-ARE 信号通路实现的。
