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Abstract
The transplantation of isolated islets is believed to be an attractive approach for
cure of diabetes mellitus. Heat-shock protein (HSP70), which plays a vital role in
cellular protection, has been detected in various tissues subjected to stress. Glutamine
(GLN) is an important cellular fuel and an essential precursor for the antioxidant
glutathione (GSH). It is believed to enhance cellular survival against a variety of
stressful stimuli through HSP70. Thus, we performed this study to examine the hypothesis
that preoperative GLN administration induces HSP70 and GSH expression before islet
transplantation attenuating ischemic damage to rat islets.
Adult male Sprague-Dawley (SD) rats were randomly divided into two groups according
to the administration of GLN after islet isolation. Group A served as the controls,
receiving no GLN. Group B islet cells were cultured with L-GLN (10 mmol/L) supplementation
for 24 hours. The GSH levels were measured in islet cells. Both HSP70 and proteins
related to apoptosis were analyzed in islet cells by Western blots. Isolated rat islets
were cultured with interleukin (IL)-1beta. Nitrite production was measured using the
Griess reagent.
The GSH levels were significantly elevated in the glutamine-treated group. HSP70 expression
in islets treated with GLN was markedly stronger compared with the control group.
The basal Bcl-2 expression was markedly increased by GLN treatment. The GLN-treated
group showed attenuated IL-1beta-induced injury in association with NO production.
These results suggested that preoperative GLN administration induced HSP70 and GSH
expressions before islet transplantation, thus attenuating IL-1beta-induced injury
in association with NO production and apoptosis, which might be potential tool to
mitigate the ischemic damage to islet cells and the early inflammation at the site
of implantation through a self-protective mechanism.