Objective: To assess the therapeutic effect of Caspase-1 inhibitor on liver injury in experimental severe acute pancreatitis (SAP). Methods: Forty-two SD rats were randomly divided into 3 groups: healthy controls (HC,...Objective: To assess the therapeutic effect of Caspase-1 inhibitor on liver injury in experimental severe acute pancreatitis (SAP). Methods: Forty-two SD rats were randomly divided into 3 groups: healthy controls (HC, n=6); SAP-S group (n=18); SAP-ICE-I group (n=18). SAP was induced by retrograde infusion of 5% sodium taurocholate into the bili-pancreatic duct in SD rats. HC rats underwent same surgical procedures and duct cannulation without sodium taurocholate. In SAP-S group, rats received the first intraperitoneal injection of isotonic saline 2 h after induction of acute pancreatitis, which was repeated after 12 h. In SAP-ICE-I group, rats were firstly given ICE inhibitor intraperitoneally 2 h after induction of pancreatitis. As in SAP-S group, this was repeated at 12 h. Survied rats were killed at certain time points, and all samples were obtained for subsequent analysis. Results: The serum levels of ALT, AST and IL-1β in SAP-S group were (215.50±58.52)U/L, (372.17±38.05)U/L, (276.77±44.92)pg/ml at 6 h, (396.67±70.29)U/L, (548.50±75.29)U/L, (308.99±34.95)pg/ml at 12 h, (425.17±86.33)U/L, (665.83±84.05)U/L, (311.60±46.51)pg/ml, respectively, which were increased significantly (P<0.01, vs HC). In SAP-ICE-I group, their levels were decreased significantly (P<0.01, vs SAP-S). Intrahepatic expressions of Caspase-1, IL-1β and IL-18 mRNA could be observed in HC, which were increased significantly in SAP-S group (P<0.01, vs HC). The expressions of IL-1β and IL-18 mRNA were decreased significantly in SAP-ICE-I group (P<0.01, vs SAP-S), whereas Caspase-1 mRNA expressions had no significant differences (P>0.05). Caspase-1 inhibition had no effect on the severity of liver tissue damage. Conclusion: Caspase-1 activate cytokines, IL-1β and IL-18, play a pivotal role in the course of liver injury in SAP. Caspase-1 inhibitor can improve liver functions effectively.展开更多
Objective: To investigate the status of cagE gene of Helicobacter pylori(H. pylori) isolated from patients with various gastrointestinal diseases and its relationship with the pathological inflammation grade and level...Objective: To investigate the status of cagE gene of Helicobacter pylori(H. pylori) isolated from patients with various gastrointestinal diseases and its relationship with the pathological inflammation grade and levels of IL 8 in the gastric mucosa and IL 8 secretion in gastric epithelial cells stimulated by H. pylori . Methods: cagE was amplified by polymerase chain reaction (PCR) in 145 clinical isolates. The inflammation grade of gastric mucosa was evaluated pathologically. IL 8 levels of gastric mucosa and IL 8 concentration of the supernatant of the cocultured SGC 7 901 cells and H. pylori was assayed by enzyme linked immunosorbent assay (ELISA). Results: cagE was positive in 79.3% of all the H. pylori strains. The mean score of the cagE positive gastritis in the antrum and corpus was (1.865±0.335) and (1.759±0.310). Meanwhile, the cagE negative grade was (1.689±0.294), (1.608±0.284). There was no significant difference ( P >0 05). The mean levels of IL 8 in cagE positive group in antrum and corpus were (390.6±101.4) pg/mg and (368.6±91.2) pg/mg; and cagE negative group were (328.6±102.8) pg/mg and (332.6±96.7) pg/mg. IL 8 in SGC7901 cells induced by cagE positive and negative group averaged (789.5±146.7) pg/ml and (757.6±136.4) pg/ml. There was still no significant difference( P >0.05). Conclusion: Positive rate of cagE is very high in Chinese patients regardless of the clinical outcome. And there was no direct relationship between cagE gene and the inflammation grade and IL 8 levels of H. pylori infected gastric mucosa and IL 8 secretion in gastric epithelial cells stimulated by H. pylori .展开更多
Objective: To study the relationship between nitric oxide synthase (NOS) expression in human gastric mucosa and Helicobacter pylori (H.pylori) infection. Methods: Gastric mucosa samples were obtained from antrum of 33...Objective: To study the relationship between nitric oxide synthase (NOS) expression in human gastric mucosa and Helicobacter pylori (H.pylori) infection. Methods: Gastric mucosa samples were obtained from antrum of 33 patients received gastroendoscopy. H.pylori infection was confirmed by Giems staining and bacteria culture under microaerophilic conditions. Expression of iNOS, eNOS and nitrotyrosine were detected by immunohistochemistry. Results: (1) The positive rate of H. pylori infection was 66.7%(22/33). (2) iNOS positive staining in inflammatory cells was detected in 77.3%(17/22) of samples with H.pylori and 27.3%(3/11) without H.pylori infection (P<0.01). (3) eNOS expression in inflammatory cells was found in 77.3%(17/22) of samples with H. pylori and 18.2%(2/11) without H.pylori infection (P<0.01). (4) Nitrotyrosine expression in inflammatory cells was observed in 59.1%(13/22) of samples with H. pylori and 54.5%(6/11) without H. pylori infection (P>0.05). (5) Moderate and severe infiltrations of inflammatory cells were found in 86.4%(19/22) of gastric biopsies with H. pylori and 9.1%(1/11) of samples without H. pylori infection (P<0.01). Conclusion: H.pylori infection might promote infiltration of mononuclear cells and macrophages in gastric mucosa and induce iNOS expression in these cells. The accumulated nitric oxide in local area may result in gastric mucosa damage.展开更多
文摘Objective: To assess the therapeutic effect of Caspase-1 inhibitor on liver injury in experimental severe acute pancreatitis (SAP). Methods: Forty-two SD rats were randomly divided into 3 groups: healthy controls (HC, n=6); SAP-S group (n=18); SAP-ICE-I group (n=18). SAP was induced by retrograde infusion of 5% sodium taurocholate into the bili-pancreatic duct in SD rats. HC rats underwent same surgical procedures and duct cannulation without sodium taurocholate. In SAP-S group, rats received the first intraperitoneal injection of isotonic saline 2 h after induction of acute pancreatitis, which was repeated after 12 h. In SAP-ICE-I group, rats were firstly given ICE inhibitor intraperitoneally 2 h after induction of pancreatitis. As in SAP-S group, this was repeated at 12 h. Survied rats were killed at certain time points, and all samples were obtained for subsequent analysis. Results: The serum levels of ALT, AST and IL-1β in SAP-S group were (215.50±58.52)U/L, (372.17±38.05)U/L, (276.77±44.92)pg/ml at 6 h, (396.67±70.29)U/L, (548.50±75.29)U/L, (308.99±34.95)pg/ml at 12 h, (425.17±86.33)U/L, (665.83±84.05)U/L, (311.60±46.51)pg/ml, respectively, which were increased significantly (P<0.01, vs HC). In SAP-ICE-I group, their levels were decreased significantly (P<0.01, vs SAP-S). Intrahepatic expressions of Caspase-1, IL-1β and IL-18 mRNA could be observed in HC, which were increased significantly in SAP-S group (P<0.01, vs HC). The expressions of IL-1β and IL-18 mRNA were decreased significantly in SAP-ICE-I group (P<0.01, vs SAP-S), whereas Caspase-1 mRNA expressions had no significant differences (P>0.05). Caspase-1 inhibition had no effect on the severity of liver tissue damage. Conclusion: Caspase-1 activate cytokines, IL-1β and IL-18, play a pivotal role in the course of liver injury in SAP. Caspase-1 inhibitor can improve liver functions effectively.
文摘Objective: To investigate the status of cagE gene of Helicobacter pylori(H. pylori) isolated from patients with various gastrointestinal diseases and its relationship with the pathological inflammation grade and levels of IL 8 in the gastric mucosa and IL 8 secretion in gastric epithelial cells stimulated by H. pylori . Methods: cagE was amplified by polymerase chain reaction (PCR) in 145 clinical isolates. The inflammation grade of gastric mucosa was evaluated pathologically. IL 8 levels of gastric mucosa and IL 8 concentration of the supernatant of the cocultured SGC 7 901 cells and H. pylori was assayed by enzyme linked immunosorbent assay (ELISA). Results: cagE was positive in 79.3% of all the H. pylori strains. The mean score of the cagE positive gastritis in the antrum and corpus was (1.865±0.335) and (1.759±0.310). Meanwhile, the cagE negative grade was (1.689±0.294), (1.608±0.284). There was no significant difference ( P >0 05). The mean levels of IL 8 in cagE positive group in antrum and corpus were (390.6±101.4) pg/mg and (368.6±91.2) pg/mg; and cagE negative group were (328.6±102.8) pg/mg and (332.6±96.7) pg/mg. IL 8 in SGC7901 cells induced by cagE positive and negative group averaged (789.5±146.7) pg/ml and (757.6±136.4) pg/ml. There was still no significant difference( P >0.05). Conclusion: Positive rate of cagE is very high in Chinese patients regardless of the clinical outcome. And there was no direct relationship between cagE gene and the inflammation grade and IL 8 levels of H. pylori infected gastric mucosa and IL 8 secretion in gastric epithelial cells stimulated by H. pylori .
基金National Natural Science Foundation of China (No.30170427)
文摘Objective: To study the relationship between nitric oxide synthase (NOS) expression in human gastric mucosa and Helicobacter pylori (H.pylori) infection. Methods: Gastric mucosa samples were obtained from antrum of 33 patients received gastroendoscopy. H.pylori infection was confirmed by Giems staining and bacteria culture under microaerophilic conditions. Expression of iNOS, eNOS and nitrotyrosine were detected by immunohistochemistry. Results: (1) The positive rate of H. pylori infection was 66.7%(22/33). (2) iNOS positive staining in inflammatory cells was detected in 77.3%(17/22) of samples with H.pylori and 27.3%(3/11) without H.pylori infection (P<0.01). (3) eNOS expression in inflammatory cells was found in 77.3%(17/22) of samples with H. pylori and 18.2%(2/11) without H.pylori infection (P<0.01). (4) Nitrotyrosine expression in inflammatory cells was observed in 59.1%(13/22) of samples with H. pylori and 54.5%(6/11) without H. pylori infection (P>0.05). (5) Moderate and severe infiltrations of inflammatory cells were found in 86.4%(19/22) of gastric biopsies with H. pylori and 9.1%(1/11) of samples without H. pylori infection (P<0.01). Conclusion: H.pylori infection might promote infiltration of mononuclear cells and macrophages in gastric mucosa and induce iNOS expression in these cells. The accumulated nitric oxide in local area may result in gastric mucosa damage.
