Expression of monocyte chemoattractant protein-1 in the pancreas of mice / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Type 1 diabetes has been recognized as an organ specific autoimmune disease owing to the immune destruction of pancreatic islet beta cells in genetically susceptible individuals. In both human and rodent models of type 1 diabetes, such as nonobese diabetic (NOD) mice, biobreeding rats, the disease has a distinct stage characterized by immune cells infiltrating in the pancreas (insulitis). The major populations of infiltrating cells are macrophages and T lymphocytes. Therefore, immune cell infiltration of pancreatic islets may be a crucial step in the pathogenesis of type 1 diabetes. Monocyte chemoattractant protein-1 can specifically attract monocytes in vivo. Interferon induced protein-10 has chemoattractant effects on the activated lymphocytes. In this study, we analysed the expression of monocyte chemoattractant protein-1 in the pancreas of mice and interferon inducible protein-10 mRNA in the pancreas of NOD mice, and discussed their possible role in the pathogenesis of type 1 diabetes.</p><p><b>METHODS</b>The immunohistochemical method and immunoelectronmicroscopy were used to evaluate the expression of monocyte chemoattractant protein-1 in the pancreas of NOD mice and BALB/c mice. RT-PCR was used to evaluate the expression of monocyte chemoattractant protein-1 and interferon inducible protein mRNA in NOD mice.</p><p><b>RESULTS</b>Monocyte chemoattractant protein-1 was positive in the pancreas of NOD mice, whereas negative in the pancreas of BALB/C mice. RT-PCR showed that monocyte chemoattractant protein-1 and interferon inducible protein-10 mRNA could be found in the pancreas of NOD mice. Immunoelectronmicroscopy demonstrated that monocyte chemoattractant protein-1 was produced by beta cells and stored in the cytoplasm of the cells.</p><p><b>CONCLUSIONS</b>Pancreatic islet beta cells produce monocyte chemoattractantprotein-1 in NOD mice. Monocyte chemoattractant protein-1 may play an important part in the pathogenesis of type 1 diabetes by attracting monocytes/macrophages to infiltrate pancreatic islets.</p>

Influence of Dexamethasone on Ultrastructure of Renal Cells in Rats with Endotoxemia / 实用儿科临床杂志

Objective To explore the mechanism of endotoxemic injury in kidneys and protective effect of dexamethasone on renal cells.Methods Fifty-four eighteen-day Wistar rats were divided into control,endotoxemic(LPS)and dexamethasone groups randomly,18 rats in every group.Rats in control group were injected intraperitoneally with the same volume(0.1 mL)of 9 g/L sodium chloride as other two groups.All rats in LPS group were injected with a single bolus of LPS(4 mg/kg).The rats in dexamethasone group received LPS(4 mg/kg)and dexamethasone(5 mg/kg).Then they were sacrificed at 6,24 and 72 hours after injection.The ultrastructure was observed by electron microscope.Results In LPS group,glomerular basement membrane became thick and foot processes had coalescent partly,mitochondrial cristae became dissolved in proximal tubular endothelial cells and microvillus of distal tubular diminished at 6,24 hours after LPS injection.The morphological changes of apoptosis were found in the proximal tubular at 72 hours after LPS injection.These changes were in dexamethasone group.Conclusion Apoptosis participates in LPS injury of kidneys and dexamethasone have protective effect on injuried renal cells.