Abstract
The antioxidative capacity of endomorphins (EMs), endogenous μ-opioid receptor agonists,
has been demonstrated by in vivo assays. In this study, we attempt to evaluate the effects of endomorphin 1 (EM1)
and endomorphin 2 (EM2) on pancreatic islet injuries induced by streptozotocin (STZ),
alloxan (ALX) and H2O2, respectively. Wistar rats’ islets were isolated and purified. The function of the
islet cells, the insulin response to glucose stimulation was examined by insulin Radio
Immuno Assay and the cell viability was measured by MTT assay. DNA fragments were
performed to evaluate the apoptosis, while the cell cycle distribution was analyzed
by PI staining flow cytometric analysis. Furthermore, the islet were treated with
EM1, EM2 or ALX for 24 h, and the expression of p53 and p21 protein were determined
by Western blot. The results showed that STZ, ALX, and H2O2 displayed clear concentration-dependent inhibitory effects on the pancreatic islet
cells. While EMs improved the viability of islet induced by STZ, ALX or H2O2, and EMs enhanced insulin accumulation of the cell supernatant after ALX and STZ
stimulation. Our data also showed both that EMs inhibited cell apoptosis and cell
cycle G1 arrest induced by STZ and ALX through down-regulaing p53 and p21 expression.
Taken together, these results demonstrate that EMs can protect islet cells from STZ,
ALX and H2O2 induced injuries. Our observations imply that the endomorphins may have protective
effects on islet cells oxidative injury.
Key words
endomorphins - pancreatic islets - oxidative damage - apoptosis
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Correspondence
J. Liu
People's Hospital of Gansu Province Endocrinology
Donggang xilu 160
Lanzhou
730000 Lanzhou
China
Email: tlm6666@sina.com