Conclusion
These results suggest that melatonin-induced upregulation of telomerase activity can interfere with mitochondrial metabolism and inhibit NLRP3 inflammasome activation in macrophages. This indicates a potential therapeutic role for melatonin in the treatment of pneumonia. Understanding the molecular mechanisms underlying these effects may lead to the development of novel therapeutic strategies targeting mitochondria and NLRP3 inflammasome activation for the management of pneumonia. Further investigations are warranted to fully uncover the therapeutic potential of melatonin and its implications for pneumonia treatment.
Methods
Macrophages were treated with melatonin to assess its impact on telomerase activity. Mitochondrial function was evaluated through the measurement of reactive oxygen species (ROS) levels and cellular energy production. NLRP3 inflammasome activation was assessed by examining the production of inflammatory cytokines, such as interleukin-1β (IL-1β). The expression levels of key proteins involved in mitochondrial metabolism and NLRP3 inflammasome signaling were also analyzed.
Objective
This study aims to investigate the effects of melatonin-induced upregulation of telomerase activity on mitochondrial metabolism and NLRP3 inflammasome activation in macrophages, with the ultimate goal of elucidating potential therapeutic implications for pneumonia treatment. Materials and
Results
Our findings demonstrated that melatonin treatment significantly upregulated telomerase activity in macrophages. This was associated with a reduction in ROS levels and enhanced cellular energy production, indicating improved mitochondrial function. Moreover, melatonin treatment suppressed NLRP3 inflammasome activation, resulting in reduced secretion of IL-1β. The expression levels of proteins involved in mitochondrial metabolism and NLRP3 inflammasome signaling were modulated by melatonin.