Rotavirus diarrhea is a major worldwide cause of infantile gastroenteritis; however, the mechanism responsible for intestinal fluid loss remains unclear. Water transfer across the intestinal epithelial membrane seems ...Rotavirus diarrhea is a major worldwide cause of infantile gastroenteritis; however, the mechanism responsible for intestinal fluid loss remains unclear. Water transfer across the intestinal epithelial membrane seems to occur because of aquaporins(AQPs). Accumulating evidence indicates that alterations in AQPs may play an important role in pathogenesis. Here, we focus on changes in AQPs in a mouse model of rotavirus diarrhea. In the present study, 32 of 35 mice developed diarrhea and mild dehydration within 24 hours after infection with rotavirus strain SA11. Intestinal epithelial cells demonstrated cytoplasmic vacuolation, malaligned villi, and atrophy. AQP1 expression was significantly attenuated in the ileum and colon in comparison with controls; likewise, AQP4 and-8 protein expression were significantly decreased in the colon of rotavirus diarrhea-infected mice. In contrast, AQP3 protein expression was significantly increased in the colon of rotavirus-infected mice in comparison with controls. These results indicate that rotavirus diarrhea is associated with the downregulation of AQP1,-4, and-8 expression. Therefore, AQPs play an important role in rotavirus diarrhea.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
Objective: To investigate the effect of Shenfu Injection (SF, ginesenoside and aconite alkaloid) on the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion in rats and its potential mechanisms...Objective: To investigate the effect of Shenfu Injection (SF, ginesenoside and aconite alkaloid) on the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion in rats and its potential mechanisms. Methods: Ischemia-reperfusion model was established in rats. Twenty-four rats were divided into 3 groups with 8 rats in each, eg, ischemia-reperfusion (I/R) group, SF-treated group, and control group. In both SF and I/R groups, the superior mesenteric artery was closed with forceps for 1 hour and then reperfused for 2 hours. Either SF (3 ml/kg, SF group) or normal saline (I/R and control groups) was injected intravenously and continuously for (5 ml/kg) with a micropump before the superior mesenteric artery was closed. The superior mesenteric artery was not closed for animals in control group. The expression of casapse-3 and Fas, and the level of TNF-α and pathological changes of the ileal mucosal tissue were assayed. Results: (1) The number of apoptosis cells increased obviously in I/R group and was significantly higher than that in SF and control groups (P<(0.05)). (2) The expression of caspase-3, Fas, and TNF-α was significantly higher in I/R group than SF and control groups (P<(0.01)); however, there was not significant difference in the expression of capase-3 between control group and SF group. There was a positive correlation between the expression of caspase-3, Fas, and TNF-α, and the number of apoptosis cells. (3) Under light microscope, intestinal mucosal impairment was found milder in SF group than (I/R) group (P<(0.05)). Conclusions: SF can depress the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion by restraining the expression of TNF-α, Fas, caspase-3, and accordingly alleviate the ischemia and reperfusion injury of intestinal mucosal epithelial cells.展开更多
基金supported by funding from Guangdong Natural Science Foundation (grants:S2012010009211,S2012010009538)Key Specialty Projects of Guangzhou Board of Health (grant:20121A021014)
文摘Rotavirus diarrhea is a major worldwide cause of infantile gastroenteritis; however, the mechanism responsible for intestinal fluid loss remains unclear. Water transfer across the intestinal epithelial membrane seems to occur because of aquaporins(AQPs). Accumulating evidence indicates that alterations in AQPs may play an important role in pathogenesis. Here, we focus on changes in AQPs in a mouse model of rotavirus diarrhea. In the present study, 32 of 35 mice developed diarrhea and mild dehydration within 24 hours after infection with rotavirus strain SA11. Intestinal epithelial cells demonstrated cytoplasmic vacuolation, malaligned villi, and atrophy. AQP1 expression was significantly attenuated in the ileum and colon in comparison with controls; likewise, AQP4 and-8 protein expression were significantly decreased in the colon of rotavirus diarrhea-infected mice. In contrast, AQP3 protein expression was significantly increased in the colon of rotavirus-infected mice in comparison with controls. These results indicate that rotavirus diarrhea is associated with the downregulation of AQP1,-4, and-8 expression. Therefore, AQPs play an important role in rotavirus diarrhea.
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.
文摘Objective: To investigate the effect of Shenfu Injection (SF, ginesenoside and aconite alkaloid) on the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion in rats and its potential mechanisms. Methods: Ischemia-reperfusion model was established in rats. Twenty-four rats were divided into 3 groups with 8 rats in each, eg, ischemia-reperfusion (I/R) group, SF-treated group, and control group. In both SF and I/R groups, the superior mesenteric artery was closed with forceps for 1 hour and then reperfused for 2 hours. Either SF (3 ml/kg, SF group) or normal saline (I/R and control groups) was injected intravenously and continuously for (5 ml/kg) with a micropump before the superior mesenteric artery was closed. The superior mesenteric artery was not closed for animals in control group. The expression of casapse-3 and Fas, and the level of TNF-α and pathological changes of the ileal mucosal tissue were assayed. Results: (1) The number of apoptosis cells increased obviously in I/R group and was significantly higher than that in SF and control groups (P<(0.05)). (2) The expression of caspase-3, Fas, and TNF-α was significantly higher in I/R group than SF and control groups (P<(0.01)); however, there was not significant difference in the expression of capase-3 between control group and SF group. There was a positive correlation between the expression of caspase-3, Fas, and TNF-α, and the number of apoptosis cells. (3) Under light microscope, intestinal mucosal impairment was found milder in SF group than (I/R) group (P<(0.05)). Conclusions: SF can depress the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion by restraining the expression of TNF-α, Fas, caspase-3, and accordingly alleviate the ischemia and reperfusion injury of intestinal mucosal epithelial cells.
