PDF(Pubmed)
Abstract：
Copper (Cu) is an essential trace element for maintaining normal homeostasis in living organisms. Yet, an elevated level of Cu beyond homeostatic capacity may lead to oxidative damage of cellular components in several organs, including the lungs. This work investigated the effects of curcumin (Curc) and nano-curcumin (nCurc) against Cu-induced lung injury, accenting the roles of oxidative stress, inflammation, and the nuclear factor erythroid 2-related factor/heme oxygenase-1 Nrf2/HO-1 pathway. Rats were challenged with 100 mg/kg of copper sulfate (CuSO4) while being treated with Curc or nCurc for 7 days. Cu-triggered lung oxidative stress detected as dysregulation of oxidative/antioxidant markers, a downregulation of Nrf-2/HO-1 signaling, and an increase in the inflammatory markers interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and intracellular adhesion molecule-1 (ICAM-1). Additionally, it decreased the expression of lung-specific proteins, surfactant protein-C (SP-C), and mucin-1 (MUC-1), induced apoptosis, and caused changes in lung histology. Curc and nCurc alleviated CuSO4-induced lung injury by suppressing oxidative damage and inflammation and activating Nrf-2/HO-1. They also prevented apoptosis and restored the normal expression of SP-C and MUC-1. We concluded that nCurc exhibited superior efficacy compared with Curc in mitigating CuSO4-induced lung injury. This was associated with reduced oxidative stress, inflammation, and apoptotic responses and increased Nrf2/HO-1 signaling and expression of SP-C and MUC-1.
摘要：
铜（Cu）是维持生物体正常稳态的必需微量元素。然而，超过稳态能力的铜水平升高可能导致几个器官细胞成分的氧化损伤，包括肺.这项工作研究了姜黄素（Curc）和纳米姜黄素（nCurc）对Cu诱导的肺损伤的作用。强调氧化应激的作用，炎症,和核因子红细胞2相关因子/血红素加氧酶-1Nrf2/HO-1通路。用100mg/kg硫酸铜(CuSO4)攻击大鼠,同时用Curc或nCurc处理7天。铜触发的肺氧化应激被检测为氧化/抗氧化标志物的失调，Nrf-2/HO-1信令的下调，和炎症标志物白细胞介素-6（IL-6）的增加，肿瘤坏死因子-α（TNF-α），和细胞内粘附分子-1(ICAM-1)。此外,它降低了肺特异性蛋白的表达，表面活性剂蛋白-C（SP-C），和粘蛋白-1（MUC-1），诱导细胞凋亡，导致肺组织学改变.Curc和nCurc通过抑制氧化损伤和炎症反应以及激活Nrf-2/HO-1减轻CuSO4诱导的肺损伤。它们还阻止了细胞凋亡并恢复了SP-C和MUC-1的正常表达。我们得出的结论是，与Curc相比，nCurc在减轻CuSO4引起的肺损伤方面表现出更好的疗效。这与减少氧化应激有关，炎症,和凋亡反应以及Nrf2/HO-1信号传导和SP-C和MUC-1的表达增加。
