Casein Glycomacropeptide Hydrolysates Exert Cytoprotective Effect against Cellular Oxidative Stress by Up-Regulating HO-1 Expression in HepG2 Cells.
Casein Glycomacropeptide Hydrolysates Exert Cytoprotective Effect against Cellular Oxidative Stress by Up-Regulating HO-1 Expression in HepG2 Cells.
复制标题
酪蛋白糖巨肽水解物通过上调 HepG2 细胞中 HO-1 的表达来发挥针对细胞氧化应激的细胞保护作用
作者：
Li T;Chen B;Du M;Song J;Cheng X;Wang X;Mao X
氧化应激被认为是代谢紊乱进展的重要介质。本研究旨在探讨牛酪蛋白糖巨肽水解物(GHP)对过氧化氢(H_2O_2)诱导的肝细胞氧化损伤的保护作用及其机制。结果表明，GHP以剂量依赖的方式显著抑制H_2O_2诱导的细胞内ROS生成和细胞存活率下降。此外，GHP浓度依赖地诱导血红素加氧酶-1(HO-1)的表达，并增加核因子-红系相关因子2(Nrf2)的核转位。此外，GHP可促进p38丝裂原活化蛋白激酶(P38 MAPK)和细胞外信号调节蛋白激酶1/2(ERK1/2)的活化，从而促进Nrf2介导的HO-1的表达。综上所述，GHP通过p38MAPK和ERK1/2信号通路激活Nrf2和HO-1，从而保护HepG2细胞免受氧化应激的影响。我们的研究结果表明，牛酪蛋白糖巨肽水解物可能是一种治疗氧化应激相关疾病的潜在成分，其体内保护作用还需要进一步研究。
Oxidative stress is considered as an important mediator in the progression of metabolic disorders. The objective of this study was to investigate the potential hepatoprotective effects and mechanisms of bovine casein glycomacropeptide hydrolysates (GHP) on hydrogen peroxide (H2O2)-induced oxidative damage in HepG2 cells. Results showed that GHP significantly blocked H2O2-induced intracellular reactive oxygen species (ROS) generation and cell viability reduction in a dose-dependent manner. Further, GHP concentration-dependently induced heme oxygenase-1 (HO-1) expression and increased nuclear factor-erythroid 2-related factor 2 (Nrf2) nuclear translocation. Moreover, pretreatment of GHP increased the activation of p38 mitogen-activated protein kinase (p38 MAPK) and extracellular signal-regulated protein kinase 1/2 (ERK1/2), which were shown to contribute to Nrf2-mediated HO-1 expression. Taken together, GHP protected HepG2 cells from oxidative stress by activation of Nrf2 and HO-1 via p38 MAPK and ERK1/2 signaling pathways. Our findings indicate that bovine casein glycomacropeptide hydrolysates might be a potential ingredient in the treatment of oxidative stress-related disorders and further studies are needed to investigate the protective effects in vivo.