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Objective To investigate changes in number of endothelial progenitor cells(EPCs)from bone marrow and circulation in mice with acute pancreatitis.Methods BALB/c mice were assigned randomly to saline group and cerulein group.Animals were sacrificed at 12, 24 and 48 hours after injection.Bone marrow and circulating EPCs were detected by flow cyzometric analysis.Plasma VEGF, TNF-α and ET-1 were determined by enzyme-linked immunosorbent assay.The expression of VEGF in the pancreas was assessed by Western blotting.Apoptosis in situ was detected by TUNEL.Results The amounts of EPCs in bone marrow and circulation increased remarkably after cerulein injection(P < 0.05), also the levels of plasma VEGF TNF-α and ET-1(P < 0.05), the EPCs levels in bone marrow and circulation seen in the study closely mirrors the levels of VEGF detected in the circulation(r = 0.77, 0.67 individually).VEGF expression in pancreas was up-regulated after 12 h of cerulein injection compared with that of control group.Apoptosis of endothelial cells also increased in the cerulein group.Conclusion EPCs were mobilized by acute pancreatitis, which may be due to the mobilizing effect of increased levels of VEGF, EPCs may participate in the repair process of injured endothelium induced by acute pancreatitis.
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Objective To study the relationship between graft-versus-host disease (GVHD) and endothelium injury following hematopoietic stem cells transplantation in mice. Methods C57BL/6 mice as donors and Balb/c mice as recipients were randomly divided into 4 groups: control group, bone marrow transplantation group, GVHD group, GVHD mitigation group. The clinical manifestations,circulating endothelial cells and tissue pathological changes were observed at different time points after transplantation. Results No manifestations of GVHD were found in each group at the day 5, while those were found in GVHD group at the day 9 and all died within 15 days. The counts of endothelial cells in peripheral blood showed no significant difference at the day 5 between GVHD group (7. 34 ±1.26 cells/μl) and bone marrow transplantation group (11.51 ± 7. 40 cells/μl) or GVHD mitigation group (7. 36 ± 0. 16 cells/μl), while among three groups there was statistically significant difference at the day 9 (GVHD group: 153. 64 ± 35. 35 cells/μl vs bone marrow transplantation group: 10. 49 ±5. 61 cells/μl and GVHD mitigation group: 47. 82 ± 4. 69 cells/μl). The scores of pathological aGVHD had no significant difference at the day 5 between GVHD group (4. 33± 1. 53) and bone marrow transplantation group (3. 33 ± 0. 58) or GVHD mitigation group (4. 00 ± 1.73), while among three groups there was statistically significant difference at the day 9 (GVHD group: 10. 0 vs bone marrow transplantation group: 3. 33 ± 1.15 or GVHD mitigation group: 4. 33 ± 0. 58) and at the day 14 (GVHD group: 10. 33 ± 2. 58 vs bone marrow transplantation group: 2. 33 ± 1.25 or GVHD mitigation group 3. 33 ± 1.15). Conclusion Occurrence of GVHD causes endothelial damage again and injured endothelium worsens the GVHD.
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AIM:To investigate COX-2 and iNOS protein contents and their interaction in vascular endothelium injury of rats with deficiency of vital energy or qi stagnation,and the prevetion and treatment of Tongxinluo.METHODS:The model of vascular endothelium injury of rats with deficiency of vital energy or qi stagnation was established by using high L-Methionine,with load-carrying swimming or being fastened respectively.Western blotting was used to analyze protein contents of COX-2 and iNOS,co-immunoprecipitation and laser confocal microscopy were used to analyze the interaction between COX-2 and iNOS.Optical microscope and electronic microscope were used to evaluate pathological changes in vascular endothelium.RESULTS:The protein contents of COX-2 and iNOS,and their interaction increased significantly in deficiency of vital energy group and qi stagnation group,in accord with injury of vascular endothelium.Compared with deficiency of vital energy group and qi stagnation group respectively,their protein contents decreased and their interaction was weakened in Tongxinluo groups.CONCLUSION:When protein contents of COX-2 and iNOS increase and their interaction enhance after vascular endothelium injury of rats with deficiency of vital energy or qi stagnation,initiate exacerbations,Tongxinluo could attenuate the alterations and protect vascular endothelium from injury.
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Objective:To investigate the relation between the angiotensinⅡ(AngⅡ)levels in thoracic aorta and plasma and atherosclerosis(AS).Methods:Totally40healthy male Wistar rats were randomly divided into4groups(n=10).Four different feeding methods,including normal diet,high lipid,high lipid+vitamin D overload,and high lipid+vitamin D over-load+endothelium injury,were used for inducing AS in rats.The thickness of intima was taken as the index of AS severity, radio-immunity analysis was used to assay AngⅡin each group in thoracic aorta and plasma.Results:Only rats in high lipid diet group did not develop AS plaque;high lipid+vitamin D only resulted in AS fibrous plaque with VSMC proliferation;high lipid+vitamin D+endothelium injury formed ripe AS plaque.The thickness of intima and AngⅡof thoracic aorta in-creased gradually compared with control group(P