Comparative evaluation of cellular senescence in naturally aged and stress-induced murine macrophages for identifying optimum senescent macrophage study systems.

Background: The role and relevance of macrophages both as causes and therapeutics of cellular senescence is rapidly emerging. However, current knowledge regarding the extent and depth of senescence in macrophages in vivo is limited and controversial. Further, acute models of stress-induced senescence in transformed/cancerous macrophage cell lines are being used although their efficacy and relevance are not characterized.

Leupeptin maintains redox homeostasis via targeting ROS-autophagy-inflammatory axis in LPS-stimulated macrophages and cytokines dichotomy in Con-A challenged lymphocyte.

Information regarding cellular anti-inflammatory and immunomodulatory attributes of leupeptin with respect to modulation of perturbed macrophage function and lymphocytes has not yet been delineated, particularly in the context of ROS-cytokines-autophagy-inflammatory signalling cascades. Therefore, the present study identified the attributes and mechanisms of leupeptin, from actinomycetes, in relation to excessive oxidative stress mediated disrupted immune homeostasis and inflammatory mechanism in activated macrophages and lymphocytes. Results revealed that leupeptin treatment showed noticeable inhibition in the production of NO, ROS, mitochondrial membrane potential and phagocytosis activity in LPS-stimulated macrophages.