School of Life Sciences, Anhui Key Laboratory of Modern Biomanufacturing, Anhui University, Hefei 230601, Anhui, PR China.
School of Life Sciences, Anhui Key Laboratory of Modern Biomanufacturing, Anhui University, Hefei 230601, Anhui, PR China.
Int J Biol Macromol. 2018 Dec;120(Pt A):865-875. doi: 10.1016/j.ijbiomac.2018.08.148. Epub 2018 Aug 29.
Oxidative stress is considered to involve cell death in severe pulmonary diseases like idiopathic pulmonary fibrosis (IPF). Polysaccharide FMP-1 from Morchella esculenta can exert significant antioxidant activity. However, its effects on alveolar epithelial cells remain unperceived. Herein, the effects of FMP-1 against HO-induced oxidative damage in human alveolar epithelial A549 cells were investigated. FMP-1 could inhibit HO-induced cytochrome C and Caspase-3 release to prevent cell apoptosis via attenuation of MDA and ROS levels, and enhancement the enzymatic activities of SOD and T-AOC. Furthermore, the underlying molecular mechanisms were clarified. The phosphorylation of AKT and the nuclear translocation of Nrf2 were observed to be promoted by FMP-1 as well as the level of HO-1. These findings suggested that FMP-1 attenuate cellular oxidative stress through PI3K/AKT pathway, and FMP-1 could be explored as natural potential antioxidants to lower oxidative stress relevant to the progression of IPF.
氧化应激被认为涉及特发性肺纤维化 (IPF) 等严重肺部疾病中的细胞死亡。从羊肚菌中提取的多糖 FMP-1 具有显著的抗氧化活性。然而,其对肺泡上皮细胞的影响尚不清楚。本研究旨在探讨 FMP-1 对 HO 诱导的人肺泡上皮 A549 细胞氧化损伤的作用。FMP-1 可通过降低 MDA 和 ROS 水平、增强 SOD 和 T-AOC 的酶活性,抑制 HO 诱导的细胞色素 C 和 Caspase-3 释放,从而防止细胞凋亡。此外,还阐明了潜在的分子机制。结果表明,FMP-1 可促进 AKT 的磷酸化和 Nrf2 的核转位,以及 HO-1 的水平。这些发现表明,FMP-1 通过 PI3K/AKT 通路减轻细胞氧化应激,FMP-1 可作为天然潜在的抗氧化剂,降低与 IPF 进展相关的氧化应激。