Akanchha Mani Tripathi, Jyoti and Nabo Kumar Chaudhury
Background: Intentional and accidentally exposure of high dose ionizing radiation results in short and long term effects in biological system. Immune
cells are vulnerable to radiation induced cell death in mature lymphocytes and precursor of monocyte and granulocyte in bone marrow.
Depletion of mature immune cells, which together defend against microbial invasion leads to the massive cell death from the infection. Need to
development of immunomodulatory drug to accelerate the recovery of immune system after radiation exposure. Our aim is to study the immunomodulatory
role of sesamol after radiation induced immunosuppression.
Methods: C57BL/6 mice were exposed to 7.5 Gy of whole body irradiation (Co60Ƴ-irradiation source) and sesamol was orally administered 30min
prior to irradiation. Mice were sacrificed on Day 1 and 14 after radiation exposure and isolate all lymphoid organ. Proliferation of bone marrow
derived mononuclear and stem cells were analysed by flowcytometry. Expression of cell surface marker of Th and Tc cells was measured in blood
and spleen cells. Activation of peritoneal macrophages was analysed by morphological observation and cell surface marker of MHC I and MHC
II. Expression of anti-inflammatory protein was observed in intestine
Results: Pre-administration of sesamol reduced the genotoxicity in bone marrow and spleen cells and maintained organ index. Sesamol balance
the T cell homeostasis in peripheral blood and spleenocyte cells by ameliorate the proliferation of the myeloid stem cell in bone marrow.
it reduced the activation of M2 type of macrophages and expression of MHC protein which directly impact on downregulating and secretory
anti-inflammatory protein COX-2, INOS and IL-6 in intestine. Collectively, these findings demonstrated immunomodulatory role of Sesamol for
maintaining the homeostasis of the immune system after radiation exposure.
Pharmacologic inhibition of XOR resulted in improved vascular and cardiac function. These results indicate, in this/these models of obesity, UA is
not causative of metabolic dysfunction whereas elevated XOR activity does alter cardiovascular function.
