A useful helicobacter pylori-induced gastritis model using BALB/c mice was established for mimicking of human gastritis induced by Helicobacter pylori (H. pylori). The H. pylori isolates were obtained freshly from a...A useful helicobacter pylori-induced gastritis model using BALB/c mice was established for mimicking of human gastritis induced by Helicobacter pylori (H. pylori). The H. pylori isolates were obtained freshly from a human complex ulcer patient. BALB/c mice were fasted for 24 h and then 0.25 mL of 0.2 mol·L -1 NaHCO 3 was administered after by gavage to each mouse and 0.5 mL of 10 9 colonies formation unit per milliliter (CFU/mL) of H. pylori was administered 15 min. On the 3 rd day and 5 th day, the H. pylori inoculations were repeated. The inoculated mice were sacrificed in batch on the 5 th day, in the 2 nd week, 3 rd week and 4 th week. The gastric mucous membrane near pyloric portion was removed, treated and then cultured under microaerobic condition for detection of H.pylori. The remainders of the gastric membrane were fixed by 10% formaldehyde solution for pathological detection. The results showed that the H. pylori could be separated from the gastric membranes of inoculated mice. Obvious invasion of inflammatory cells in the gastric membranes of inoculated mice could be observed from pathological sections. It can be concluded that the inoculating fresh human H. pylori isolates can produce mouse gastritis. This model of BALB/c mice can be used for evaluating the therapeutic agents for the treatment of gastritis induced by H. pylori.展开更多
Objective: To survey the effects of inhaled heparin on airway inflammation inguinea pigs with asthma and investigate the possible mechanism of inhaled heparin in the treatmentof asthma. Methods: The asthma in guinea p...Objective: To survey the effects of inhaled heparin on airway inflammation inguinea pigs with asthma and investigate the possible mechanism of inhaled heparin in the treatmentof asthma. Methods: The asthma in guinea pigs induced by ovalbumin was treated with inhaled heparin.The changes of cellularities in bronchoalveolar lavage (BAL) fluid and the airway walls wereexamined. Histologic examinations were also done in the guinea pig controls. Results: The number ofeosinophils, lymphocytes, and ciliated epithelial cells in the BAL fluid from the group treated withheparin was significantly lower than that of the group of asthma controls (P<0.01). Within theairway watts of the heparin treated group, the eosinophil infiltration was less prominent than thatof the group of asthma controls (P<0.001) and the number of mast cell was significantly higher thanthat of the group of asthma controls (P<0.01). Histologic examination showed that airway damages inthe heparin treated group were mild. Conclusion: Heparin can inhibit airway inflammation andalleviate airway damage in guinea pigs with asthma.展开更多
AIM: To investigate the therapeutic effect of tetrandrine on liver fibrosis induced by thioacetamide in rats in vivo and in vitro. METHODS: In vitro study: we investigated the effect of tetrandrine on the apoptosis...AIM: To investigate the therapeutic effect of tetrandrine on liver fibrosis induced by thioacetamide in rats in vivo and in vitro. METHODS: In vitro study: we investigated the effect of tetrandrine on the apoptosis of rat hepatic stellate cells transformed by simian virus 40 (T-HSC/CI-6), which retains the features of activated cells. In vivo study: hepatic fibrosis was induced in rats by thioacetamide. Tetrandrine was given orally to rats at doses of 5, 10 or 20 mg/kg for 4 wk compared with intraperitoneal injection of interferon-r. RESULTS: In vitro study: 5, 10 or 25 μg/mL of tetrandrine-induced activation of caspase-3 in t-HSC/CI-6 cells occurred dose-dependently. In vivo study: tetrandrine treatment as well as interferon-r significantly ameliorated the development of fibrosis as determined by lowered serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (T-Bil) and the levels of liver hydroxyproline (Hyp), hyaluronic acid (HA), laminin (LN) and also improved histological findings. The effects of tetrandrine at the concentration of 20 mg/kg were better than the other concentration groups. CONCLUSION: Tetrandrine promotes the apoptosis of activated HSCs in vitro. Tetrandrine administration can prevent liver fibrosis and liver damage induced by thioacetamide in rats in vivo, indicating that it might exert a direct effect on rat HSCs.展开更多
AIM: To investigate the hypothesis that the protective effects of curcumin in hepatic warm ischemia/reperfusion (I/R) injury are associated with increasing heat shock protein 70 (Hsp70) expression and antioxidant...AIM: To investigate the hypothesis that the protective effects of curcumin in hepatic warm ischemia/reperfusion (I/R) injury are associated with increasing heat shock protein 70 (Hsp70) expression and antioxidant enzyme activity. METHODS: Sixty Sprague-Dawley male rats were randomly divided into sham, I/R, C + I/R groups. The model of reduced-size liver warm ischemia and reperfusion was used. Curcumin (50 mg/kg) was administered by injection through a branch of superior mesenteric vein at 30 min before ischemia in C + I/R group. Five rats were used to investigate the survival during 1 wk after operation in each group. Blood samples and liver tissues were obtained in the remaining animals after 3, 12, and 24 h of reperfusion to assess serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), liver tissue NO2- + NO3-, malondialdehyde (MDA) content, superoxide dismutase (SOD), catalase (CAT), nitricoxide synthase (NOS) and myeloperoxidase (MPO) activity, HspT0 expression and apoptosis ratio. RESULTS: Compared with I/R group, curcumin pretreatment group showed less ischemia/reperfusioninduced injury. CAT and SOD activity and Hsp70 expression increased significantly. A higher rate of apoptosis was observed in I/R group than in C + I/R group, and a significant increase of MDA, NO2^- + NO3^- and MPO level in liver tissues and serum transaminase concentration was also observed in I/R group compared to C + I/R group. Curcumin also decreased the activity of inducible NO synthase (iNOS) in liver after reperfusion,but had no effect on the level of endothelial NO synthase (eNOS) after reperfusion in liver. The 7 d survival rate was significantly higher in C + I/R group than in I/R group. CONCLUSION: Curcumin has protective effects against hepatic I/R injury. Its mechanism might be related to the overexpression of Hsp70 and antioxidant enzymes.展开更多
AIM:To establish a gastric cancer nude-mouse model with improved orthotopic implantation and investigate its biological characteristics at different time points.METHODS:Human gastric cancer SGC-7901 cell suspensions w...AIM:To establish a gastric cancer nude-mouse model with improved orthotopic implantation and investigate its biological characteristics at different time points.METHODS:Human gastric cancer SGC-7901 cell suspensions were injected subcutaneously into a nude mouse to develop solid tumors,and the tumor tissue pieces were implanted under the serous coat.The nude mice were then euthanized in group every two weeks to observe the primary tumor growth and metastases.RESULTS:Within 2-4 wk,there were no obvious chang-es about the primary tumor in stomach.At the sixth week,the primary tumor began to grow fast,resulting in incrassation of the gastric wall and stenosis of the gastric cavity,and metastases into the liver and lymph nodes were detected.The tumor,which compressed the adjacent organs,gradually became bigger and bigger followed by stenosis or vanishment of the gastric cavity from 8 to 12 wk.There were massive metastases,and the rate of metastasis was 58%in lymph nodes,78%in liver,39%in kidney,and 81%in peritoneum or septum.CONCLUSION:A gastric cancer model is established,which can simulate the clinical tumor behavior and provide experimental carrier for clinical trials of gastric cancer treatment.展开更多
AIM:To investigate the correlation of hyperlipemia(HL) and acute cerebral ischemia/reperfusion(I/R) injury on liver damage and its mechanism.METHODS:Rats were divided into 4 groups:control,HL,I/R and HL+I/R.After the ...AIM:To investigate the correlation of hyperlipemia(HL) and acute cerebral ischemia/reperfusion(I/R) injury on liver damage and its mechanism.METHODS:Rats were divided into 4 groups:control,HL,I/R and HL+I/R.After the induction of HL via a high-fat diet for 18 wk,middle cerebral artery occlusion was followed by 24 h of reperfusion to capture I/R.Serum alanine transaminase(ALT) and aspartate aminotransferase(AST) were analyzed as part of liver function tests and liver damage was further assessed by histological examination.Hepatocyte apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL) assay.The expression of genes related to apoptosis(caspase-3,bcl-2) was assayed by immunohistochemistry and Western blotting.Serum tumor necrosis factor-(TNF-),interleukin-1(IL-1) and liver mitochondrial superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),malondialdehyde(MDA) and Ca 2+ levels were measured to determine inflammatory and oxidative/antioxidative status respectively.Microsomal hydroxylase activity of the cytochrome P450 2E1(CYP2E1)-containing enzyme was measured with aniline as the substrate,and CYP2E1 expression in the liver tissue and microsome was determined by immunohistochemistry and Western blotting respectively.RESULTS:HL alone induced by high-fat diet for 18 wk resulted in liver damage,indicated by histopathological analysis,and a considerable increase in serum ALT(25.13 ± 16.90 vs 9.56 ± 1.99,P < 0.01) and AST levels(18.01 ± 10.00 vs 11.33 ± 4.17,P < 0.05) compared with control.Moreover,HL alone induced hepatocyte apoptosis,which was determined by increased TUNEL-positive cells(4.47 ± 0.45 vs 1.5 ± 0.22,P < 0.01),higher caspase-3 and lower bcl-2 expression.Interestingly,compared with those in control,HL or I/R groups,massive increases of serum ALT(93.62 ± 24.00 vs 9.56 ± 1.99,25.13 ± 16.90 or 12.93 ± 6.14,P < 0.01) and AST(82.32 ± 26.92 vs 11.33 ± 4.17,18.01 ± 10.00 or 14.00 ± 6.19,P < 0.01) levels in HL+I/R group were observed suggesting severe liver damage,which was confirmed by liver histology.In addition,HL combined with I/R also caused significantly increased hepatocyte apoptosis,as evidenced by increased TUNEL-positive cells(6.20 ± 0.29 vs 1.5 ± 0.22,4.47 ± 0.45 or 1.97 ± 0.47,P < 0.01),elevated expression of caspase-3 and lower expression of bcl-2.Furthermore,when compared to HL or I/R alone,HL plus I/R enhanced serum TNF-,IL-1,liver mitochondrial MDA and Ca 2+ levels,suppressed SOD and GSH-Px in liver mitochondria,and markedly up-regulated the activity(11.76 ± 2.36 vs 4.77 ± 2.31 or 3.11 ± 1.35,P < 0.01) and expression(3.24 ± 0.38 vs 1.98 ± 0.88 or 1.72 ± 0.58,P < 0.01) of CYP2E1 in liver.CONCLUSION:The coexistence of HL and acute cerebral I/R induces severe liver damage,suggesting that cerebral ischemic stroke would exaggerate the damage of liver caused by HL.This effect is possibly due to en-hanced CYP2E1 induction which further promotes oxidative damage,inflammation and hepatocyte apoptosis.展开更多
Objective: To improve the method of pancreaticoduodenal transplantation and to establish a more physiological rat model. Methods: SD rats served as donors and recipients. The vein was reconstructed by end-to-side anas...Objective: To improve the method of pancreaticoduodenal transplantation and to establish a more physiological rat model. Methods: SD rats served as donors and recipients. The vein was reconstructed by end-to-side anastomosis between the donor portal vein and the recipient superior mesenteric vein, and arterial reconstruction was carried out by end-to-side anastomosis of the donor to the recipient abdominal aorta. Enteric drainage was performed by side-to-side anastomosis between the duodenum of donors and that of recipients. Results: Fifty experiments were performed. The successful rate of transplantation which restored the recipients euglycemia were 78%. Conclusion: This model of pancreaticoduodenal transplantation in rats was stable and reliable, which was in accordance with the trend of clinical pancreas transplantation and could be applied for further scientific research.展开更多
AIM: To observe the effect of resveratrol on nuclear factor Kappa-B (NF-κB) activation and the inflammatory response in sodium taurocholate-induced pancreatitis in rats. METHODS: Seventy-two male SD rats were randoml...AIM: To observe the effect of resveratrol on nuclear factor Kappa-B (NF-κB) activation and the inflammatory response in sodium taurocholate-induced pancreatitis in rats. METHODS: Seventy-two male SD rats were randomly divided into three groups: sham operation group (control), severe acute pancreatitis (SAP) group, and severe acute pancreatitis group treated with resveratrol (RES). A SAP model was established by injecting 4% sodium taurocholate 1 mL/kg through puncturing the pancreatic duct. In Res group, Res was given at 30 mg/kg b.m. intraperitoneally after the SAP model was successfully established. Eight animals from each group were sacrificed at 3, 6 and 12 h after modeling. The expression of NF-κB activation of pancreas was detected by irnmunohistochemical staining, whereas the levels of TNF-α and IL-8 in pancreatic tissues were estimated by radioimrnunoassay. The pathological changes of pancreas and lungs were examined microscopically. RESULTS: Much less hyperemia, edema, dust-colored necrotic focus and soaps were noticed in pancreas in RES group than in SAP group. In RES group, hemorrhage, exudates and infiltration of inflammatory cells in pancreas and interstitial edema, destruction of alveolar wall in lung were significantly less than in SAP group. In the SAP group, the activation of NF-κB in pancreatic tissues was enhanced significantly at any measure point compared with control group (64.23±10.72% vs 2.56±0.65%, 55.86±11.34% vs 2.32±0.42%, 36.23±2.30% vs 2.40±0.36%,P<0.01), TNF-α, IL-8 were also increased and reached their peak at 6 h and then declined. The activation of NF-κB and the levels of TNF-α and IL-8 in RES group were significantly lower than those in SAP group (P<0.01): activation (52.63±9.45% vs 64.23±10.72%, 40.52±8.40% vs 55.86±11.34%, 29.83±5.37% vs 36.23±2.30%), TNF-α (132.76±15.68 pg/mL vs 158.36±12.58 pg/mL, 220.32±23.57 pg/mL vs 247.67± 11.62 pg/mL, 175.68±18.43 pg/mL vs 197.35±12.57 pg/mL) and IL-8 (0.62±0.21 μg/L vs 0.83±0.10 μg/L, 1.10±0.124 μg/L vs1.32±0.18 μg/L, 0.98±0.16 μg/L vs 1.27±0.23μg/L). CONCLUSION: The activation of NF-KB is involved in the inflammatory response of rats with SAP. Resveratrol could effectively inhibit the expression of NF-κB activation, alleviate the severity of SAP through its anti-inflammatory effects and regulate the inflammatory mediators.展开更多
AIM: To study the stability of portal hypertension (PHT) caused by partial ligation of the portal vein ligation (PVL) in a rat model.METHODS: Thirty male adult Wistar rats were divided into two groups: 10 in Gr...AIM: To study the stability of portal hypertension (PHT) caused by partial ligation of the portal vein ligation (PVL) in a rat model.METHODS: Thirty male adult Wistar rats were divided into two groups: 10 in Group Ⅰ received a sham operation; and 20 in Group Ⅱreceived partial PVL. Portal vein pressure (PVP) was measured at four time periods: before ligation, 2 wk, 6 wk and 10 wk postsurgery. Portal venography, blood sampling and liver and spleen pathological examinations were conducted at 10 wk after surgery.RESULTS: The PVP was 9.15± 0.58 cmH2O before ligation, and increased to 17.32 ±0.63 cmH2O 2 wk after PVL. By repeat measurement of the PVP in each rat, it was shown to remain elevated for 10 wk. There were no significant differences in the pressure measurements at 2 wk, 6 wk and 10 wk. Varices were found mainly in the mesenteric vein 2 wk after PVL, which were more obvious later, while these manifestations were similar at week 6 and week 10. Portal venography demonstrated the varices and collaterals. There was no significant change in liver pathology. The volume of the spleen was enlarged 2-fold after ligation, and the sinus of the spleen was enlarged due to congestion. Significant sinus endothelial cell proliferation was observed, but no evidence of hypersplenia was found on hemogram and biochemical examination.CONCLUSION: These findings suggest that a satisfactory prehepatic PHT rat model can be obtained by partial ligation of the portal vein, and this PHT rat model was stable for at least 10 wk.展开更多
文摘A useful helicobacter pylori-induced gastritis model using BALB/c mice was established for mimicking of human gastritis induced by Helicobacter pylori (H. pylori). The H. pylori isolates were obtained freshly from a human complex ulcer patient. BALB/c mice were fasted for 24 h and then 0.25 mL of 0.2 mol·L -1 NaHCO 3 was administered after by gavage to each mouse and 0.5 mL of 10 9 colonies formation unit per milliliter (CFU/mL) of H. pylori was administered 15 min. On the 3 rd day and 5 th day, the H. pylori inoculations were repeated. The inoculated mice were sacrificed in batch on the 5 th day, in the 2 nd week, 3 rd week and 4 th week. The gastric mucous membrane near pyloric portion was removed, treated and then cultured under microaerobic condition for detection of H.pylori. The remainders of the gastric membrane were fixed by 10% formaldehyde solution for pathological detection. The results showed that the H. pylori could be separated from the gastric membranes of inoculated mice. Obvious invasion of inflammatory cells in the gastric membranes of inoculated mice could be observed from pathological sections. It can be concluded that the inoculating fresh human H. pylori isolates can produce mouse gastritis. This model of BALB/c mice can be used for evaluating the therapeutic agents for the treatment of gastritis induced by H. pylori.
文摘Objective: To survey the effects of inhaled heparin on airway inflammation inguinea pigs with asthma and investigate the possible mechanism of inhaled heparin in the treatmentof asthma. Methods: The asthma in guinea pigs induced by ovalbumin was treated with inhaled heparin.The changes of cellularities in bronchoalveolar lavage (BAL) fluid and the airway walls wereexamined. Histologic examinations were also done in the guinea pig controls. Results: The number ofeosinophils, lymphocytes, and ciliated epithelial cells in the BAL fluid from the group treated withheparin was significantly lower than that of the group of asthma controls (P<0.01). Within theairway watts of the heparin treated group, the eosinophil infiltration was less prominent than thatof the group of asthma controls (P<0.001) and the number of mast cell was significantly higher thanthat of the group of asthma controls (P<0.01). Histologic examination showed that airway damages inthe heparin treated group were mild. Conclusion: Heparin can inhibit airway inflammation andalleviate airway damage in guinea pigs with asthma.
基金the National Natural Science Foundation of China, No. 32060127 and No. 30660225
文摘AIM: To investigate the therapeutic effect of tetrandrine on liver fibrosis induced by thioacetamide in rats in vivo and in vitro. METHODS: In vitro study: we investigated the effect of tetrandrine on the apoptosis of rat hepatic stellate cells transformed by simian virus 40 (T-HSC/CI-6), which retains the features of activated cells. In vivo study: hepatic fibrosis was induced in rats by thioacetamide. Tetrandrine was given orally to rats at doses of 5, 10 or 20 mg/kg for 4 wk compared with intraperitoneal injection of interferon-r. RESULTS: In vitro study: 5, 10 or 25 μg/mL of tetrandrine-induced activation of caspase-3 in t-HSC/CI-6 cells occurred dose-dependently. In vivo study: tetrandrine treatment as well as interferon-r significantly ameliorated the development of fibrosis as determined by lowered serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (T-Bil) and the levels of liver hydroxyproline (Hyp), hyaluronic acid (HA), laminin (LN) and also improved histological findings. The effects of tetrandrine at the concentration of 20 mg/kg were better than the other concentration groups. CONCLUSION: Tetrandrine promotes the apoptosis of activated HSCs in vitro. Tetrandrine administration can prevent liver fibrosis and liver damage induced by thioacetamide in rats in vivo, indicating that it might exert a direct effect on rat HSCs.
文摘AIM: To investigate the hypothesis that the protective effects of curcumin in hepatic warm ischemia/reperfusion (I/R) injury are associated with increasing heat shock protein 70 (Hsp70) expression and antioxidant enzyme activity. METHODS: Sixty Sprague-Dawley male rats were randomly divided into sham, I/R, C + I/R groups. The model of reduced-size liver warm ischemia and reperfusion was used. Curcumin (50 mg/kg) was administered by injection through a branch of superior mesenteric vein at 30 min before ischemia in C + I/R group. Five rats were used to investigate the survival during 1 wk after operation in each group. Blood samples and liver tissues were obtained in the remaining animals after 3, 12, and 24 h of reperfusion to assess serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), liver tissue NO2- + NO3-, malondialdehyde (MDA) content, superoxide dismutase (SOD), catalase (CAT), nitricoxide synthase (NOS) and myeloperoxidase (MPO) activity, HspT0 expression and apoptosis ratio. RESULTS: Compared with I/R group, curcumin pretreatment group showed less ischemia/reperfusioninduced injury. CAT and SOD activity and Hsp70 expression increased significantly. A higher rate of apoptosis was observed in I/R group than in C + I/R group, and a significant increase of MDA, NO2^- + NO3^- and MPO level in liver tissues and serum transaminase concentration was also observed in I/R group compared to C + I/R group. Curcumin also decreased the activity of inducible NO synthase (iNOS) in liver after reperfusion,but had no effect on the level of endothelial NO synthase (eNOS) after reperfusion in liver. The 7 d survival rate was significantly higher in C + I/R group than in I/R group. CONCLUSION: Curcumin has protective effects against hepatic I/R injury. Its mechanism might be related to the overexpression of Hsp70 and antioxidant enzymes.
基金Supported by the Natural Science Foundation of China,No. 30830040
文摘AIM:To establish a gastric cancer nude-mouse model with improved orthotopic implantation and investigate its biological characteristics at different time points.METHODS:Human gastric cancer SGC-7901 cell suspensions were injected subcutaneously into a nude mouse to develop solid tumors,and the tumor tissue pieces were implanted under the serous coat.The nude mice were then euthanized in group every two weeks to observe the primary tumor growth and metastases.RESULTS:Within 2-4 wk,there were no obvious chang-es about the primary tumor in stomach.At the sixth week,the primary tumor began to grow fast,resulting in incrassation of the gastric wall and stenosis of the gastric cavity,and metastases into the liver and lymph nodes were detected.The tumor,which compressed the adjacent organs,gradually became bigger and bigger followed by stenosis or vanishment of the gastric cavity from 8 to 12 wk.There were massive metastases,and the rate of metastasis was 58%in lymph nodes,78%in liver,39%in kidney,and 81%in peritoneum or septum.CONCLUSION:A gastric cancer model is established,which can simulate the clinical tumor behavior and provide experimental carrier for clinical trials of gastric cancer treatment.
文摘AIM:To investigate the correlation of hyperlipemia(HL) and acute cerebral ischemia/reperfusion(I/R) injury on liver damage and its mechanism.METHODS:Rats were divided into 4 groups:control,HL,I/R and HL+I/R.After the induction of HL via a high-fat diet for 18 wk,middle cerebral artery occlusion was followed by 24 h of reperfusion to capture I/R.Serum alanine transaminase(ALT) and aspartate aminotransferase(AST) were analyzed as part of liver function tests and liver damage was further assessed by histological examination.Hepatocyte apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL) assay.The expression of genes related to apoptosis(caspase-3,bcl-2) was assayed by immunohistochemistry and Western blotting.Serum tumor necrosis factor-(TNF-),interleukin-1(IL-1) and liver mitochondrial superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),malondialdehyde(MDA) and Ca 2+ levels were measured to determine inflammatory and oxidative/antioxidative status respectively.Microsomal hydroxylase activity of the cytochrome P450 2E1(CYP2E1)-containing enzyme was measured with aniline as the substrate,and CYP2E1 expression in the liver tissue and microsome was determined by immunohistochemistry and Western blotting respectively.RESULTS:HL alone induced by high-fat diet for 18 wk resulted in liver damage,indicated by histopathological analysis,and a considerable increase in serum ALT(25.13 ± 16.90 vs 9.56 ± 1.99,P < 0.01) and AST levels(18.01 ± 10.00 vs 11.33 ± 4.17,P < 0.05) compared with control.Moreover,HL alone induced hepatocyte apoptosis,which was determined by increased TUNEL-positive cells(4.47 ± 0.45 vs 1.5 ± 0.22,P < 0.01),higher caspase-3 and lower bcl-2 expression.Interestingly,compared with those in control,HL or I/R groups,massive increases of serum ALT(93.62 ± 24.00 vs 9.56 ± 1.99,25.13 ± 16.90 or 12.93 ± 6.14,P < 0.01) and AST(82.32 ± 26.92 vs 11.33 ± 4.17,18.01 ± 10.00 or 14.00 ± 6.19,P < 0.01) levels in HL+I/R group were observed suggesting severe liver damage,which was confirmed by liver histology.In addition,HL combined with I/R also caused significantly increased hepatocyte apoptosis,as evidenced by increased TUNEL-positive cells(6.20 ± 0.29 vs 1.5 ± 0.22,4.47 ± 0.45 or 1.97 ± 0.47,P < 0.01),elevated expression of caspase-3 and lower expression of bcl-2.Furthermore,when compared to HL or I/R alone,HL plus I/R enhanced serum TNF-,IL-1,liver mitochondrial MDA and Ca 2+ levels,suppressed SOD and GSH-Px in liver mitochondria,and markedly up-regulated the activity(11.76 ± 2.36 vs 4.77 ± 2.31 or 3.11 ± 1.35,P < 0.01) and expression(3.24 ± 0.38 vs 1.98 ± 0.88 or 1.72 ± 0.58,P < 0.01) of CYP2E1 in liver.CONCLUSION:The coexistence of HL and acute cerebral I/R induces severe liver damage,suggesting that cerebral ischemic stroke would exaggerate the damage of liver caused by HL.This effect is possibly due to en-hanced CYP2E1 induction which further promotes oxidative damage,inflammation and hepatocyte apoptosis.
文摘Objective: To improve the method of pancreaticoduodenal transplantation and to establish a more physiological rat model. Methods: SD rats served as donors and recipients. The vein was reconstructed by end-to-side anastomosis between the donor portal vein and the recipient superior mesenteric vein, and arterial reconstruction was carried out by end-to-side anastomosis of the donor to the recipient abdominal aorta. Enteric drainage was performed by side-to-side anastomosis between the duodenum of donors and that of recipients. Results: Fifty experiments were performed. The successful rate of transplantation which restored the recipients euglycemia were 78%. Conclusion: This model of pancreaticoduodenal transplantation in rats was stable and reliable, which was in accordance with the trend of clinical pancreas transplantation and could be applied for further scientific research.
基金Supported by the National Natural Science Foundation of China, No.30371398
文摘AIM: To observe the effect of resveratrol on nuclear factor Kappa-B (NF-κB) activation and the inflammatory response in sodium taurocholate-induced pancreatitis in rats. METHODS: Seventy-two male SD rats were randomly divided into three groups: sham operation group (control), severe acute pancreatitis (SAP) group, and severe acute pancreatitis group treated with resveratrol (RES). A SAP model was established by injecting 4% sodium taurocholate 1 mL/kg through puncturing the pancreatic duct. In Res group, Res was given at 30 mg/kg b.m. intraperitoneally after the SAP model was successfully established. Eight animals from each group were sacrificed at 3, 6 and 12 h after modeling. The expression of NF-κB activation of pancreas was detected by irnmunohistochemical staining, whereas the levels of TNF-α and IL-8 in pancreatic tissues were estimated by radioimrnunoassay. The pathological changes of pancreas and lungs were examined microscopically. RESULTS: Much less hyperemia, edema, dust-colored necrotic focus and soaps were noticed in pancreas in RES group than in SAP group. In RES group, hemorrhage, exudates and infiltration of inflammatory cells in pancreas and interstitial edema, destruction of alveolar wall in lung were significantly less than in SAP group. In the SAP group, the activation of NF-κB in pancreatic tissues was enhanced significantly at any measure point compared with control group (64.23±10.72% vs 2.56±0.65%, 55.86±11.34% vs 2.32±0.42%, 36.23±2.30% vs 2.40±0.36%,P<0.01), TNF-α, IL-8 were also increased and reached their peak at 6 h and then declined. The activation of NF-κB and the levels of TNF-α and IL-8 in RES group were significantly lower than those in SAP group (P<0.01): activation (52.63±9.45% vs 64.23±10.72%, 40.52±8.40% vs 55.86±11.34%, 29.83±5.37% vs 36.23±2.30%), TNF-α (132.76±15.68 pg/mL vs 158.36±12.58 pg/mL, 220.32±23.57 pg/mL vs 247.67± 11.62 pg/mL, 175.68±18.43 pg/mL vs 197.35±12.57 pg/mL) and IL-8 (0.62±0.21 μg/L vs 0.83±0.10 μg/L, 1.10±0.124 μg/L vs1.32±0.18 μg/L, 0.98±0.16 μg/L vs 1.27±0.23μg/L). CONCLUSION: The activation of NF-KB is involved in the inflammatory response of rats with SAP. Resveratrol could effectively inhibit the expression of NF-κB activation, alleviate the severity of SAP through its anti-inflammatory effects and regulate the inflammatory mediators.
基金Supported by National 10th 5-year Science Research Plan of China,No.2001BA705B10-15
文摘AIM: To study the stability of portal hypertension (PHT) caused by partial ligation of the portal vein ligation (PVL) in a rat model.METHODS: Thirty male adult Wistar rats were divided into two groups: 10 in Group Ⅰ received a sham operation; and 20 in Group Ⅱreceived partial PVL. Portal vein pressure (PVP) was measured at four time periods: before ligation, 2 wk, 6 wk and 10 wk postsurgery. Portal venography, blood sampling and liver and spleen pathological examinations were conducted at 10 wk after surgery.RESULTS: The PVP was 9.15± 0.58 cmH2O before ligation, and increased to 17.32 ±0.63 cmH2O 2 wk after PVL. By repeat measurement of the PVP in each rat, it was shown to remain elevated for 10 wk. There were no significant differences in the pressure measurements at 2 wk, 6 wk and 10 wk. Varices were found mainly in the mesenteric vein 2 wk after PVL, which were more obvious later, while these manifestations were similar at week 6 and week 10. Portal venography demonstrated the varices and collaterals. There was no significant change in liver pathology. The volume of the spleen was enlarged 2-fold after ligation, and the sinus of the spleen was enlarged due to congestion. Significant sinus endothelial cell proliferation was observed, but no evidence of hypersplenia was found on hemogram and biochemical examination.CONCLUSION: These findings suggest that a satisfactory prehepatic PHT rat model can be obtained by partial ligation of the portal vein, and this PHT rat model was stable for at least 10 wk.