BACKGROUNDLittle is known of the effects of hydrocortisone on cell adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and its counterreceptors (LFA-1, Mac-1) in acute pancreatitis (AP). We investigated the effects of prior treatment with hydrocortisone on the production of ICAM-1 and its counterreceptors (LFA-1 and Mac-1) in AP of rats to clarify the effect of hydrocortisone on induced acute pancreatitis.

METHODSAcute pancreatitis was induced by infusion of 5% chenodeoxycholic acid into the pancreatic duct, followed by ligation of pancreatic duct. Before induction of acute pancreatitis, rats were treated with hydrocortisone (n = 20) or 0.9% saline (n = 20). Blood and specimens from pancreas and lung were obtained from 5 rats from each treatment euthanized at 1 hour or 3 hours, 6 hours, 12 hours. Expression of ICAM-1 was assessed by immunohistochemistry and Western blot analysis of pancreas and lungs. The expression of LFA-1 and Mac-1 on neutrophils was detected by flow cytometer. The therapeutic effect of hydrocortisone was assessed from injuries to pancreas and lung.

RESULTSICAM-1 expression in the pancreas of hydrocortisone group was significantly less than in control group at 3 hours and 6 hours. In the lungs of hydrocortisone group, ICAM-1 expression was significantly less than in control group at 3 hours, 6 hours and 12 hours. The expression of LFA-1 and Mac-1 on neutrophils in blood increased significantly in control group over hydrocortisone group. Increased expression of ICAM-1, LFA-1 and Mac-1 preceded leukocyte infiltration. Compared to untreated animals with acute pancreatitis, rats pretreated with hydrocortisone had significantly reduced histological lung injury and output of ascitic fluid.

CONCLUSIONSPrior treatment with hydrocortisone before the induction of acute pancreatitis ameliorates pulmonary injury and the output of ascitic fluid and reduces the expression of ICAM-1 and its counterreceptors (LFA-1, Mac-1) in acute pancreatitis.

Acute Disease ; Amylases ; blood ; Animals ; Hydrocortisone ; pharmacology ; therapeutic use ; Intercellular Adhesion Molecule-1 ; analysis ; Lymphocyte Function-Associated Antigen-1 ; blood ; Macrophage-1 Antigen ; blood ; Pancreatitis ; blood ; drug therapy ; Rats ; Rats, Sprague-Dawley

We examined the role of cell adhesion molecules (CAM) by which tumor cells bind to the endothelial cells using human umbilical vein endothelial cells (HUVEC) and cultured melanoma cells. Endothelial cells from human umbilical veins were isolated and examined for CAM expression and its modulation by tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), interleukin-6 (IL-6) or interferon-gamma (IFN-gamma). The expression of intercellular adhesion molecule 1 (ICAM-1) on HUVEC was increased by TNF-alpha, IL-1 and IFN-gamma when measured by ELISA or flow cytometric (FACS) analysis. IL-6 did not increase ICAM-1 expression on HUVEC. Two melanoma cell lines, Malme-3M and SK-Mel-28, showed increased expression of ICAM-1 after treatment with TNF-alpha, IL-1 and IFN-gamma in FACS analysis. IFN-gamma induced increased expression of HLA-DR only in SK-Mel-28 melanoma cells, not in Malme-3M melanoma cells. Neither HUVEC nor melanoma cells expressed lymphocyte function-associated antigen 1 (LFA-1) in either the basal (i.e., cytokine untreated) condition or the cytokine treated condition. Melanoma cells showed minimal increment in adhesion to TNF-alpha or IL-1 treated HUVEC than to cytokine untreated HUVEC. HUVEC and melanoma cells did not express LFA-1 and increased ICAM-1 expression by TNF-alpha, IL-1 and IFN-gamma treatment in FACS analysis did not coincide with minimal increase of melanoma cells adhesion to cytokine treated HUVEC. These results suggest that adhesion between melanoma cells and HUVEC is probably mediated by molecular interaction other than ICAM-1/LFA-1.
Cell Adhesion/drug effects ; Cell Adhesion Molecules/*analysis ; Cell Division/drug effects ; Cells, Cultured ; Cytokines/*pharmacology ; Endothelium, Vascular/cytology/*physiology ; HLA-DR Antigens/analysis ; Humans ; Intercellular Adhesion Molecule-1 ; Lymphocyte Function-Associated Antigen-1/analysis ; Melanoma/*pathology ; Tumor Cells, Cultured

The objective of study was to investigate the effect of ligustrazine on the expression of LFA-1 and ICAM-1 in bone marrow and the mechanism of hematopoietic reconstitution after bone marrow transplantation (BMT). The 150 mice were randomly divided into 3 groups: normal group, saline group and ligustrazine group. The normal group was not treated. The saline group was given normal saline (0.2 ml/mouse, twice a day) through gastric tube, while the ligustrazine group was given ligustrazine (0.2 ml/mouse, twice a day) through gastric tube. At days 7, 14, 21 and 28 after BMT, the survival rate, colony forming unit of spleen (CFU-S), peripheral blood cells, bone marrow mononuclear cells (BMMNC), histologic changes of bone marrow, as well as the expression level of LFA-1 and ICAM-1 were observed. The results showed that in ligustrazine group CFU-S counts on day 10 and survival rate, WBC and Plt amount in peripheral blood, BMMNC counts, hematopoietic tissue volume as well as the expression level of LFA-1 at 7, 14, 21, 28 days after BMT were higher than in saline group (P < 0.01 or P < 0.05). However, mature RBC volume and expression level of ICAM-1 were lower than in the saline group (P < 0.01 or P < 0.05). Furthermore, fat tissue volume was higher at 7 and 14 days (P < 0.01) and was lower at 21 and 28 days (P < 0.01) after BMT than in the saline group. It is concluded that ligustrazine could improve bone marrow microenvironment and promote hematopoietic reconstitution.
Animals ; Blood Cell Count ; Bone Marrow Examination ; Bone Marrow Transplantation ; Female ; Intercellular Adhesion Molecule-1 ; analysis ; Lymphocyte Function-Associated Antigen-1 ; analysis ; Male ; Mice ; Mice, Inbred BALB C ; Pyrazines ; pharmacology