1) BACKGROUND: Phycocyanin (PC) is a type of natural protein in algae with antioxidant and anti-inflammatory properties. However, the protective effect of PC on hepatic damage induced by X-ray remains unknown. 2) METHODS: Male C57BL/6 mice were gavaged with 200mg/kg PC for consecutive 7 days before or after radiation. The blood samples and tissues were collected on days 1 and 7 after radiation exposure. 3) RESULTS: Pretreatment or treatment with PC decreased significantly the levels of alanine aminotransferase (ALT), aspartate aminotransferase(AST) in the plasma. Histological evaluation further confirmed the protection of PC against radiation-induced hepatotoxicity. PC-treatment also increased the relative mRNA expression of superoxide dismutase (SOD) and glutathione (GSH-PX), and descended the ROS in the liver. Moreover, the expression of H2AX, an indicator of DNA damage in mice, of the PC-intervention group was much smaller than that of the radiation group. In vivo, PC-treatment markedly up-regulated NF-E2-related factor 2(Nrf2) expression and downstream gene such as hemeoxygenase-1 (HO-1), NQO1. 4) Conclusion: PC could attenuate the radiation-induced oxidative stress damage by activating Nrf2/ HO-1 signaling pathway, and reduce the radiation-induced DNA damage. Therefore, PC is a protective agent against radiation-induced liver damage.

The prevention and treatment of chronic obstructive pulmonary disease (COPD) is closely tied to antioxidation and anti-inflammation. Phycocyanin (PC) has numerous pharmacological effects, such as antioxidation and anti-inflammation. However, it remains unclear whether PC can play a therapeutic role in COPD. As inflammation and oxidative stress can aggravate COPD, this study is to explore the effect of PC on COPD mice and its mechanisms. The COPD mice model was established by exposing them to lipopolysaccharide (LPS) and cigarette smoke (CS); PC was administrated in a concentration of 50 mg/kg for 30 days. On the last day, lung function was measured, and bronchoalveolar lavage fluid (BALF) was obtained and classified for cells. Lung tissue pathological change was analyzed, and organ indices statistics were measured. Based on molecular docking, the mechanism was explored with Western blotting, immunohistochemical, and immunofluorescence in vivo and in vitro. PC significantly ameliorated the pulmonary function of COPD mice and reduced inflammation of the lung (p < 0.05), and hematoxylin and eosin (H&E) staining showed PC depressed lung inflammatory cell accumulation and emphysema. Periodic acid Schiff (PAS) and Masson staining revealed that PC retarded goblet cells metaplasia and collagen deposition (p < 0.05). In addition, in vivo PC regulated Heme oxygenase 1 (HO-1) (p < 0.05) and NAD(P)H dehydrogenase quinone 1 (NQO1) level (p < 0.01) in the lung, as well as NOX2 level in pulmonary macrophages. Molecular docking results indicate that phycocyanobilin (PCB) in PC had a good binding site in Keap1 and NOX2 proteins; the phycocyanobilin-bound phycocyanin peptide (PCB-PC-peptide) was obtained for further studies. In vitro, PCB-PC-peptide could depress the phospho-NF-E2-related factor 2 (p-Nrf2) and NQO1 protein expression in RAW264.7 cells induced by cigarette smoke extract (CSE) (p < 0.05). PC exerts beneficial effects on COPD via anti-inflammatory and antioxidative stress, which may be achieved through PCB.