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.     

Effect of high thoracic epidural block on expression of β1-ARK mRNA in lymphocytes in elderly patients with essential hypertension complicated with left ventricular hypertrophy

Objective To investigate the effect of high thoracic epidural block (HTEB) on the expression of β-adrenergie receptor kinaseo-1 (β1-ARK) mRNA in the lymphocytes in the elderly patients with essential hypertension complicated with left ventricular hypertrophy (LVH). Methods Twenty ASA Ⅱ or Ⅲ elderly patients with essential hypertension complicated with LVH scheduled for subtotal gastrectomy under general anesthesia were randomly divided into 2 groups (n = 10 each) : intravenous-inhalational anesthesia group (group Ⅰ) and HTEB combined with intravenous-inhalational anesthesia group (group Ⅱ). In group Ⅱ , epidural anesthesia was performed at T6.7 and ropivacaine was infused until 72 h after operation for HTEB. In group Ⅰ ,patient-controlled intravenous analgesia (PCIA) was performed with fentanyl in 72 h after operation. The heart rate variability (HRV) parameters, including total power (TP), high frequency (HF) power and low frequency (LF) power, were recorded 30 min after entering the operating room (baseline), at the recovery time of consciousness (T1), and on 1st, 3rd and 5th day after operation (T2-4) ,and LF/HF was calculated. VAS scores were recorded and the severity of pain was assessed. The blood samples were drawn from the right internal jugular vein at the time points mentioned above for determination of β1-ARK mRNA and β1-arrestin mRNA expression. Resets There were no significant differences in VAS scores at each time point between two groups (P > 0.05). TP, HF, LF and LF/HF were significantly increased, and β1-ARK mRNA expression was down-regulated after operation in group Ⅱcompared with group Ⅰ (P < 0.05 or 0.01), but there was no significant difference in β1-arrestin mRNA expression between group Ⅰ and Ⅱ (P > 0.05) . TP was siguificantly increased, HF significantly decreased, and β1-ARK mRNA expression up-regulated in two groups at T2 compared with those at T1 (P < 0.05), but no significant difference was found at the other time points (P > 0.05). TP was inversely correlated with the expression of β1-ARK mRNA in the lymphocytes during the perioperative period using Pearson correlation analysis (r=-0.520, P <0.01). Conclusion HTEB can maintain the balance of the autonomic nervous system and improve HRV during upper abdominal surgery in the elderly patients with essential hypertension complicated with LVH, and the mechanism is related to the up-regulation of β1-ARK mRNA expression.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.