AIM: To describe the effect of Rheum tanguticum polysaccharide (RTP) on hydrogen peroxide-induced human intestinal epithelial cell injury. METHODS: Hydrogen peroxide (100 μmol/L) was introduced to induce human intest...AIM: To describe the effect of Rheum tanguticum polysaccharide (RTP) on hydrogen peroxide-induced human intestinal epithelial cell injury. METHODS: Hydrogen peroxide (100 μmol/L) was introduced to induce human intestinal epithelial cell injury. Cells were pretreated with RTP (30,100,300 μg/mL) for 24 h before exposure to hydrogen peroxide. Cell viability was detected by MTT assay and morphological observation. Acridine orange staining and flow cytometry were performed to assess cell apoptosis. Lactate dehydrogenase (LDH) activity, production of malondialdehyde (MDA) and superoxide dismutase (SOD) activity were measured by spectrophotometry with corresponding assay kits. RESULTS: Following exposure to H2O2, a marked decrease in cell survival and SOD activity, increased production of MDA, LDH leakage and cell apoptosis were found. Pretreatment of the cells with RTP could significantly elevate cell survival, SOD activity and decrease the level of MDA, LDH activity and cell apoptosis. CONCLUSION: RTP may have cytoprotective and anti-oxidant effects against H2O2-induced intestinal epithelial cell injury by inhibiting cell apoptosis and necrosis. This might be one of the possible mechanisms of RTP for the treatment of ulcerative colitis in rats.展开更多
AIM:To examine the influence of ghrelin on the regenerative potential of gastrointestinal(GI)epithelium.METHODS:Damage to GI epithelium was induced in mice by two intravenous injections of doxorubicin(10 and 6 mg/kg)....AIM:To examine the influence of ghrelin on the regenerative potential of gastrointestinal(GI)epithelium.METHODS:Damage to GI epithelium was induced in mice by two intravenous injections of doxorubicin(10 and 6 mg/kg).Some of the doxorubicin-treated mice received a continuous subcutaneous infusion of ghrelin(1.25μg/h)for 10 d via implanted mini-osmotic pumps.To label dividing stem cells in the S-phase of the cell cycle,all mice received a single intraperitoneal injection of 5'-bromo-2'-deoxyuridine(BrdU)one hour before sacrifice.The stomach along with the duodenum were then removed and processed for histological examination and immunohistochemistry using anti-BrdU antibody.RESULTS:The results showed dramatic damage to the GI epithelium 3 d after administration of chemotherapy which began to recover by day 10.In ghrelintreated mice,attenuation of GI mucosal damage was evident in the tissues examined postchemotherapy.Immunohistochemical analysis showed an increase in the number of BrdUlabeled cells and an alteration in their distribution along the epithelial lining in response to damage by doxorubicin.In mice treated with both doxorubicin and ghrelin,the number of BrdUlabeled cells was reduced when compared with mice treated with doxorubicin alone.CONCLUSION:The present study suggests that ghrelin enhances the regenerative potential of the GI epithelium in doxorubicintreated mice,at least in part,by modulating cell proliferation.展开更多
AIM:To study the effect of circulating cell-free oxy-hemoglobin(FHb) on intestinal microcirculation and intestinal epithelial injury in a rat model. METHODS:To induce elevated intravascular circulating FHb,male Spragu...AIM:To study the effect of circulating cell-free oxy-hemoglobin(FHb) on intestinal microcirculation and intestinal epithelial injury in a rat model. METHODS:To induce elevated intravascular circulating FHb,male Sprague-Dawley rats received water or FHb infusion.Microcirculatory changes in jejunum,ileum and colon were evaluated using fluorescent microspheres.Intestinal injury was quantified as plasmatic release of ileal lipid binding protein(iLBP) and verified by histological analysis of the ileum. RESULTS:Water and FHb infusions resulted,when compared with saline infusion,in reduced intestinal microcirculation(after 30 min P<0.05,or better;after 60 min FHb infusion P<0.05 for jejunum and colon) .Circulating FHb levels correlated significantly with release of iLBP(Spearman r=0.72,P=0.0011) .Epithelial cell injury of the villi was histologically observed after water and FHb infusions. CONCLUSION:This study shows that circulating FHb leads to a reduction in intestinal microcirculatory blood flow with marked injury to intestinal epithelial cells. These data support the hypothesis that circulating FHb contributes to the development of intestinal injury.展开更多
Objective： To evaluate the local risk factors of traumatic brain injury （TBI） patients developing gastrointestinal （GI） bleeding during the early hospitalization in neurosurgery intensive care unit （NICU）. Met...Objective： To evaluate the local risk factors of traumatic brain injury （TBI） patients developing gastrointestinal （GI） bleeding during the early hospitalization in neurosurgery intensive care unit （NICU）. Method： From September 2005 to February 2006, 41 patients admitted to NICU and 13 healthy volunteers were involved in our study. Blood samples at 24 hours, 2-3 days and 5-7 days were obtained from each patient via arterial line at 8 a.m. to measure the concentrations of serum adrenocorticotropic hormone （ACTH）, total cortisol and gastrin. The collected serum was immersed in an ice bath and tested by the Immulite 1000 systems. Data were analyzed by SPSS 11.5. Results： Within 24 hours following TBI, the concentrations of total cortisol, ACTH and gastrin increased proportionally to the severity of injury, especially significant in the experimental group （P〈0.05）. The concentrations of ACTH and gastrin were higher in the GI bleeding positive group than in the GI bleeding negative group, （F=1.413, P=0.253） for ACTH and （F=9.371, P=0.006） for gastrin. GI bleeding had a positive correlation with gastrin concentration （r=0. 312, P〈0.05） and a negative correlation with serum hemoglobin （Hb） （r=-0.420, P〈0.01）. The clinical incidence of GI bleeding was 24.39% （10/41） in the experimental group. Within 24 hours, GI bleeding had a strong correlation with gastrin concentration （OR=26.643, P〈0.05） and hematocrit （Hct） （OR=5.385, P〈0.05）. High ACTH concentration （〉100 pg/ml） increased the frequency of GI bleeding. For patients with severe TBI and treated with routine antacids, the incidence of GI bleeding was 40.91% （9/22） and the mortality rate was 20%（2/10）. Conclusions： Low Glasgow coma scale scores, low Hb, high concentrations of gastrin and ACTH （〉 100 pg/ml） are risk factors and can be predictive values for post-traumatic GI bleeding. Severe TBI patients have high risks of GI bleeding with high mortality.展开更多
基金Supported by the National Natural Science Foundation of China,No. 30100239
文摘AIM: To describe the effect of Rheum tanguticum polysaccharide (RTP) on hydrogen peroxide-induced human intestinal epithelial cell injury. METHODS: Hydrogen peroxide (100 μmol/L) was introduced to induce human intestinal epithelial cell injury. Cells were pretreated with RTP (30,100,300 μg/mL) for 24 h before exposure to hydrogen peroxide. Cell viability was detected by MTT assay and morphological observation. Acridine orange staining and flow cytometry were performed to assess cell apoptosis. Lactate dehydrogenase (LDH) activity, production of malondialdehyde (MDA) and superoxide dismutase (SOD) activity were measured by spectrophotometry with corresponding assay kits. RESULTS: Following exposure to H2O2, a marked decrease in cell survival and SOD activity, increased production of MDA, LDH leakage and cell apoptosis were found. Pretreatment of the cells with RTP could significantly elevate cell survival, SOD activity and decrease the level of MDA, LDH activity and cell apoptosis. CONCLUSION: RTP may have cytoprotective and anti-oxidant effects against H2O2-induced intestinal epithelial cell injury by inhibiting cell apoptosis and necrosis. This might be one of the possible mechanisms of RTP for the treatment of ulcerative colitis in rats.
文摘AIM:To examine the influence of ghrelin on the regenerative potential of gastrointestinal(GI)epithelium.METHODS:Damage to GI epithelium was induced in mice by two intravenous injections of doxorubicin(10 and 6 mg/kg).Some of the doxorubicin-treated mice received a continuous subcutaneous infusion of ghrelin(1.25μg/h)for 10 d via implanted mini-osmotic pumps.To label dividing stem cells in the S-phase of the cell cycle,all mice received a single intraperitoneal injection of 5'-bromo-2'-deoxyuridine(BrdU)one hour before sacrifice.The stomach along with the duodenum were then removed and processed for histological examination and immunohistochemistry using anti-BrdU antibody.RESULTS:The results showed dramatic damage to the GI epithelium 3 d after administration of chemotherapy which began to recover by day 10.In ghrelintreated mice,attenuation of GI mucosal damage was evident in the tissues examined postchemotherapy.Immunohistochemical analysis showed an increase in the number of BrdUlabeled cells and an alteration in their distribution along the epithelial lining in response to damage by doxorubicin.In mice treated with both doxorubicin and ghrelin,the number of BrdUlabeled cells was reduced when compared with mice treated with doxorubicin alone.CONCLUSION:The present study suggests that ghrelin enhances the regenerative potential of the GI epithelium in doxorubicintreated mice,at least in part,by modulating cell proliferation.
基金Supported by The Profileringsfonds of the Maastricht University Medical Center(to Jacobs MJ and Buurman WA)an AGIKO-stipendium 920-03-522(to Lubbers T)from The Netherlands Organization for Health Research and Development
文摘AIM:To study the effect of circulating cell-free oxy-hemoglobin(FHb) on intestinal microcirculation and intestinal epithelial injury in a rat model. METHODS:To induce elevated intravascular circulating FHb,male Sprague-Dawley rats received water or FHb infusion.Microcirculatory changes in jejunum,ileum and colon were evaluated using fluorescent microspheres.Intestinal injury was quantified as plasmatic release of ileal lipid binding protein(iLBP) and verified by histological analysis of the ileum. RESULTS:Water and FHb infusions resulted,when compared with saline infusion,in reduced intestinal microcirculation(after 30 min P<0.05,or better;after 60 min FHb infusion P<0.05 for jejunum and colon) .Circulating FHb levels correlated significantly with release of iLBP(Spearman r=0.72,P=0.0011) .Epithelial cell injury of the villi was histologically observed after water and FHb infusions. CONCLUSION:This study shows that circulating FHb leads to a reduction in intestinal microcirculatory blood flow with marked injury to intestinal epithelial cells. These data support the hypothesis that circulating FHb contributes to the development of intestinal injury.
文摘Objective： To evaluate the local risk factors of traumatic brain injury （TBI） patients developing gastrointestinal （GI） bleeding during the early hospitalization in neurosurgery intensive care unit （NICU）. Method： From September 2005 to February 2006, 41 patients admitted to NICU and 13 healthy volunteers were involved in our study. Blood samples at 24 hours, 2-3 days and 5-7 days were obtained from each patient via arterial line at 8 a.m. to measure the concentrations of serum adrenocorticotropic hormone （ACTH）, total cortisol and gastrin. The collected serum was immersed in an ice bath and tested by the Immulite 1000 systems. Data were analyzed by SPSS 11.5. Results： Within 24 hours following TBI, the concentrations of total cortisol, ACTH and gastrin increased proportionally to the severity of injury, especially significant in the experimental group （P〈0.05）. The concentrations of ACTH and gastrin were higher in the GI bleeding positive group than in the GI bleeding negative group, （F=1.413, P=0.253） for ACTH and （F=9.371, P=0.006） for gastrin. GI bleeding had a positive correlation with gastrin concentration （r=0. 312, P〈0.05） and a negative correlation with serum hemoglobin （Hb） （r=-0.420, P〈0.01）. The clinical incidence of GI bleeding was 24.39% （10/41） in the experimental group. Within 24 hours, GI bleeding had a strong correlation with gastrin concentration （OR=26.643, P〈0.05） and hematocrit （Hct） （OR=5.385, P〈0.05）. High ACTH concentration （〉100 pg/ml） increased the frequency of GI bleeding. For patients with severe TBI and treated with routine antacids, the incidence of GI bleeding was 40.91% （9/22） and the mortality rate was 20%（2/10）. Conclusions： Low Glasgow coma scale scores, low Hb, high concentrations of gastrin and ACTH （〉 100 pg/ml） are risk factors and can be predictive values for post-traumatic GI bleeding. Severe TBI patients have high risks of GI bleeding with high mortality.
