| Alzheimer's disease is correlated with neuronal degeneration and loss of neuronal precursors in different parts of
the brain. It has been found disturbance in the homeostasis neural stem cells (NSCs) can cause neurodegeneration.
Morphine, an analgesic agent, can disrupt the dynamic and normal state of NSCs. However, more investigations
are required to clearly address underlying mechanisms. The current experiment aimed to investigate
the effects of morphine on the cell distribution of insulin factor and receptor and insulin-like growth factors
(IGF1, IGF2) in NSCs.
NSCs were isolated from rats and stemness feature confirmed by antibodies against nestin and Sox2. The cells
were exposed to 100 μM morphine, 50 μM naloxone and combination of these two drugs for 72 h. The neural cell
growth, changes in levels of insulin and insulin-like growth factors secreted by NSCs as well as the insulinreceptor-
gene expression were assessed by flow cytometry, ELlSA, and real-time PCR, respectively.
Cell cycle assay revealed the exposure of cells to morphine for 72 h increased cell apoptosis and decreased
neural stem cell growth. The biosynthesis of insulin, insulin-like growth factors, and insulin receptor were reduced
(p < 0.05) after NSCs exposure to morphine at the concentration of 100 μM for 24, 48 and 72 h.
Naloxone is a competitive antagonist which binds MOR where morphine (and endogenous opioids) bind, and
reversed the detrimental effects of morphine.
It can be concluded that morphine initiated irregularity in NSCs kinetics and activity by reducing the secretion
of insulin and insulin-like growth factors and down-regulation of insulin receptor. |