ABSTRACT
BACKGROUND:Acute pancreatitis is a common inflammatory disease mediated by pancreatic acinar cel s injury, and is mainly characterized by leukocyte infiltration. N-acetylcysteine can control leukocyte migration and regulate inflammation in some serious inflammatory diseases. OBJECTIVE:To investigate the protective effects of N-acetylcysteine in rat model of acute pancreatitis caused by sodium taurocholate. METHODS:Ninety Sprague-Dawley rats were randomly divided into three groups:normal control group, acute pancreatitis group and N-acetylcysteine group. Except normal control group, acute pancreatitis model was established in the other two groups by retrograde injection of sodium taurocholate into major duodenal papil a. Rats in the N-acetylcysteine group were treated with N-acetylcysteine intravenously through the tail vein. RESULTS AND CONCLUSION:After acute pancreatitis model was established, plasma amylase levels in the models were significantly higher than that in the normal control rats (P<0.05). Interleukin-1β,-6,-10, and tumor necrosis factorαexpression levels were also obviously higher than that in the normal control rats (P<0.05). Immunohistochemical staining demonstrated that N-acetylcysteine was mainly expressed in the islet cel s, and the pancreatic expression of N-acetylcysteine was down-regulated at both the mRNA and protein levels during the course of acute pancreatitis. N-acetylcysteine administration significantly reduced plasma amylase levels, myeloperoxidase activity, pro-inflammatory cytokine production, and pancreas and lung tissue damages. Furthermore, N-acetylcysteine administration did not cause significant inhibition of nuclear factor-κB activation in the pancreas. N-acetylcysteine is capable of improving damage of pancreas and lung, and exerting anti-inflammatory effects in rats with severe acute pancreatitis.
ABSTRACT
BACKGROUND:Wnt signaling pathway is the key to regulation of cell proliferation and differentiation.The evidence suggests that this pathway participates in the neural precursor cell proliferation,differentiation and determination of the regulation of cell fate.At present,the Wnt signaling pathway effects on the mesenchymal stem cells(MSCs)differentiated into neuron-like cells have not been reported.OBJECTIVE:To seek Wnt signal molecule that promotes the differentiation of MSCs into neuron-like cells.METHODS:MSCs were isolated from the femur of Sprague Dawley rats in vitro using the density gradient centrifugation,and then cultured.Following passage,cell surface markers CD29,CD44,CD34 and CD45 were measured using morphology and flow cytometry.These cells were selected and evaluated.Using neurotrophic factor and basic fibroblast growth factor combined with Wnt3a and Wnt5a induction scheme,effects of Wnt3a and Wnt5a during the differentiation of MSCs into neuron-like cells were compared utilizing immunohistochemistry and reverse transcription-polymerase chain reaction(RT-PCR).Simple culture of basic fibroblast growth factor served as controls.RESULTS AND CONCLUSION:Following culture and passage of MSCs,cells adhered to the wall,showing even spindle shape.Flow cytometry showed great expression of CD29 and CD44 and low expression of CD34 and CD45.Following Wnt3a induction,cells were positive for nestin,neuron specific enolase,but no significantly expressed glial fibrillary acidic protein.Following induction,cell viability was good.In the Wnt5a induction and control groups,weakly positive expression of nestin was found,but neuron specific enolase and glial fibrillary acidic protein were negative.RT-PCR results demonstrated that nestin expression was detected in the Wnt3a induction group before and after induction.Significant amplified bands for neuron specific enolase were detected at day 5 following induction,and became more significant at day 10.Weak bands for glial fibrillary acidic protein were visible at day 10 following induction.These indicated that Wnt3a can promote the differentiation of MSCs into neuron-like cells in vitro.
ABSTRACT
BACKGROUND:In vitro experiment has shown that the survival time of conventional chemical induction-induced neuron-like cells differentiated from bone marrow mesenchymal stem cells(BMSCs)was short,which limited its further application.With regard to the possibility of extension of iodine-induced neuron-like cells,the survival time has not yet been professionally reported.OBJECTIVE:To research the effects of the micro-element iodine on the survival time of neuron-like cells differentiated by BMSCs.METHODS:Rat mesenchymal stem cells at passage 3 were obtained under sterile condition,and divided into groups A-F.In group A,iodine ion was not added.In groups B-F,iodine ion at mass concentrations of 2,55,90,125 and 2 500 mg/L was added respectively.An additional blank control group was established,and simultaneously the cells were induced into neuron-like cells with dimethyl sulphoxide(DMSO).Cells following induction were subjected to immunohistochemistry.Survival time of neuron-like cells was observed under different mass concentrations of iodine ion.RESULTS AND CONCLUSION:When mass concentrations of iodine ion were between 55-125 mg/L,the survival time of neuron-like cells prolonged to about 5 days and structures of induced cells were intact.From then on,the number of dead cells was gradually increased till approximately one week,all neuron-like cells died.When mass concentrations of iodine ion were 2 mg/L and 2 500 mg/L,cell survival time was from 12-36 hours.No significant difference was determined compared with group A.Till 2 or 3 days,all neuron-like cells died.Above-described results indicated that an appropriated concentration of iodine iron added in the common chemical induction may be benefit for the survival time of the neuron-like cells differentiated by BMSCs,but the effect may be negligible for the survival time of neuron-like cells induced when the added concentration of iodine iron is too low or too high.