No abstract

Aging has become a global public health challenge. Many studies have revealed that the excessive generation of ROS and oxidative stress could be the major causative factors contributing to aging. In this study, R-phycocyanin (R-PC) was isolated from Porphyra haitanensis, and its anti-aging ability was explored by natural aging Drosophila melanogaster and H2O2-induced HUVEC cells as the aging model. Results showed that R-PC α and β subunits expressed have antioxidant activity and can inhibit the generation of radicals, exhibiting a protective effect against H2O2-induced apoptotic HUVEC cells death. R-PC prevented the H2O2-induced HUVEC cell cycle phase arrest by regulating cell cycle-related protein. Furthermore, R-PC prevented the H2O2-induced HUVEC cell cycle phase arrest by regulating cell-cycle-related protein expression. In vivo study also indicated that R-PC significantly increased the survival time and alleviated the oxidative stress of Drosophila melanogaster. Moreover, R-PC notably decreased levels of ROS in natural aging flies and inhibited lipid peroxidation by enhancing the expressions of the endogenous stress marker genes (SOD1, SOD2, CAT of Drosophila melanogaster). Taken together, a study on the antioxidation extract from Porphyra haitanensis, such as R-PC, may open a new window for the prevention of anti-aging.

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.