Aim:
Apoptosis is a genetically programmed cell death mechanism which plays important roles in normal physiology such as tissue homeostasis regulation and pathophsiology of various diseases. iNOS enzyme activation and nitric oxide synthesis in various cell types as a defense mechanism against microbial and viral pathogens plays an important role in inflammatory and immune pathologies such as atherosclerosis, rheumatoid arthritis, diabetes, septic shock, multiple sclerosis and highly uncontrolled production of nitric oxide leads to cell death. Recently, glucosamine which is acclaimed to be beneficial for inflammatory disorders such as osteoarthritis is widely used clinically. There is limited information regarding the effect mechanisms of glucosamine on apoptosis of mainly immune cells, macrophages. In this study, effects of different concentrations of glucosamine were tested on LPS/IFNγ activated RAW 264.7 macrophages.
Materials and methods:
RAW 264.7 macrophage cell line was treated with or without glucosamine before LPS/IFNγ stimulation. Nitrite levels, cell viability, caspase-3 activity, mitochondria membrane potential and flow cytometric analysis with Annexin V-PI cell staining was performed.
Results and discussion:
Glucosamine inhibited nitrite levels, increased mitochondrial membrane potential, decreased caspase-3 enzyme activity significantly (p<0.05) and exhibited antiapoptotic effects. As the NO inhibitor effect of glucosamine on activated cells is not potent, the antiapoptotic effects of glucosamine is partly nitric oxide dependent and nitric oxide independent pathways are also thought to be responsible. In this regard, further elaborate studies are needed to clarify the effects of glucosamine on specific signaling pathways.
Keywords: Apoptosis, glucosamine, nitric oxide, macrophage
