R-phycocyanin from porphyra haitanensis attenuates apoptosis, ROS accumulation and cell cycle arrest induced by ameliorated cigarette smoke extract through AKT/MAPK/NF-κB signaling in human lung fbroblasts HFL1 cells

Abstract

The risk of human lung diseases and abnormal development under the toxic environmental exposure conditions of passive cigarette smoke is emerging. R-phycocyanin (R-PC) has health benefits for a range of lung diseases including lung injury. The goal of this study was to investigate R-PC improves cigarette smoke-induced cell apoptosis and cycle arrest and its underlying molecular mechanisms in human lung fibroblasts. The effect of R-PC on cytotoxicity, apoptosis, ΔΨm and cell cycle arrest were measured through LDH assay, Hoechst/PI staining, JC-1 assay, flow cytometry, ELISA. The mechanisms of R-PC used DCFH-DA fluorescent probe for reactive oxygen species (ROS) level and western blotting analysis for signaling. Results showed that R-PC have great anti-oxidant activity and can inhibit the generation of radicals, expressed a protective effect against CSE-induced apoptotic HFL1 cells death and cycle phase arrest. Furthermore, CSE added the level of ROS and activated p38 and JNK signaling, inhibited AKT and NF-κB signaling. Pre-treatment with R-PC inhibited CSE-induced p38, JNK phosphorylation and ROS production, activated AKT, ERK, MKK4 and NF-κB signaling pathways. The findings suggested that R-PC treatment ameliorated CSE-induced ROS accumulation, apoptosis and cell cycle arrest by AKT/MAPK/NF-κB signaling pathways in HFL1 cells.