Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

Rosiglitazone down-regulates lipopolysaccharide-induced expression of CD40 and intercellular adhesion molecule 1 in rat peritoneal mesothelial cells through a NF-κB dependent mechanism

Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献   

腹腔镜胃癌手术对腹膜间皮细胞ICAM-1和整合素β1表达的影响及意义

目的研究腹腔镜胃癌根治术中腹膜间皮细胞ICAM-1和整合素β1表达的变化,探讨腹腔镜胃癌根治术对腹膜转移的可能影响。方法选择2008年4月至8月行腹腔镜胃癌根治术的26例（腹腔镜组）和同期行开腹胃癌根治术的20例（开腹组）患者,根据手术进程分3个时相（手术开始、手术2h及4h）取右上腹膜,采用免疫组织化学方法检测腹膜间皮细胞ICAM-1和整合素β1的表达。结果随手术时间的延长,腹腔镜组与开腹组腹膜间皮细胞ICAM-1和整合素β1的阳性表达均呈逐渐增强趋势。其中手术4h时两组整合素β1的阳性表达与本组手术开始时相比,差异有统计学意义（P〈0.05）。但两种黏附分子的阳性表达在3个手术时相中,两组间的差异均无统计学意义（P〉0.05）。结论与开腹手术相比,腹腔镜胃癌根治术没有增强腹膜间皮细胞ICAM-1和整合素β1的表达。腹腔镜胃癌手术可能并未通过改变腹膜间皮细胞黏附分子的表达而促进胃癌的腹膜转移。