AIM: To study the modulation of glutamate on post-ischemic intestinal and cerebral inflammatory responses in a ischemic and excitotoxic rat model.METHODS: Adult male rats were subjected to bilateral carotid artery occ...AIM: To study the modulation of glutamate on post-ischemic intestinal and cerebral inflammatory responses in a ischemic and excitotoxic rat model.METHODS: Adult male rats were subjected to bilateral carotid artery occlusion for 15 min and injection of monosodium glutamate intraperitoneally, to decapitate them at selected time points. Tumor necrosis factor alpha (TNF-α) level and nuclear factor kappa B (NF-κB) activity were determined by enzyme-linked immunosorbant assay (ELISA) and electrophoretic mobility shift assay (EMSA), respectively.Hemodynamic parameters were monitored continuously during the whole process of cerebral ischemia and reperfusion.RESULTS: Monosodium glutamate (MSG) treated rats displayed statistically significant high levels of TNF-α in cerebral and intestinal tissuess within the first 6 h of ischemia. The rats with cerebral ischemia showed a minor decrease of TNF-α production in cerebral and intestinal tissuess. The rats with cerebral ischemia and treated with MSG displayed statistically significant low levels of TNF-α in cerebral and intestinal tissues. These results correlated significantly with NF-κB production calculated at the same intervals. During experiment, the mean blood pressure and heart rates in all groups were stable.CONCLUSION: Glutamate is involved in the mechanism of intestinal and cerebral inflammation responses. The effects of glutamate on cerebral and intestinal inflammatory responses after ischemia are up-regulated at the transcriptional level,through the NF-κB signal transduction pathway.展开更多
This experiment aimed to discuss and reveal the effect and mechanism of mannanase on intestinal inflammation in broilers triggered by a soybean meal diet.In this experiment,384 Arbor Acres broilers at1 d old were rand...This experiment aimed to discuss and reveal the effect and mechanism of mannanase on intestinal inflammation in broilers triggered by a soybean meal diet.In this experiment,384 Arbor Acres broilers at1 d old were randomly divided into 3 treatment groups.The broilers were fed a corn-soybean meal basal diet,a low-energy diet(metabolizable energy reduced by 50 kcal/kg),and a low-energy diet supplemented with 100 mg/kg mannanase for 42 d.The low-energy diet increased feed conversion ratio from0 to 42 d,reduced ileal villus height and villus height-to-crypt depth ratio and upregulated the expression of nuclear factor kappa B(NF-κB)in the ileum(P<0.05).It also reduced cecal short-chain fatty acids(SCFA),such as acetic acid(P<0.05).Compared with low-energy diets,the addition of mannanase increased body weight at 42 d,promoted the digestibility of nutrients,and maintained the morphology and integrity of the intestinal epithelium of broilers(P<0.05).In addition,mannanase upregulated the expression of claudin-1(CLDN1)and zonula occludens-1(ZO-1)in the jejunum at 21 d,downregulated the expression of ileal NF-κB,and increased the content of isobutyric acid in the cecum of broilers(P<0.05).The results for the ileal microbiota showed that a low-energy diet led to a decrease in the relative abundance of Lactobacillus reuteri in the ileum of broilers.The addition of mannanase increased the relative abundance of Lactobacillus-KC45b and Lactobacillus johnsonii in broilers.Furthermore,a low-energy diet reduced the relative abundance of Butyricicoccus in the intestine of broilers and inhibited oxidative phosphorylation and phosphoinositol metabolism.Mannanase increased the relative abundance of Odoribacter,promoted energy metabolism and N-glycan biosynthesis,and increased the activities of GH3 and GH18.It is concluded that mannanase could improve the growth performance of broilers by reducing the expression of NF-κB in the ileum,increasing the production of SCFA in the cecum,suppressing intestinal inflammation,balancing the intestinal microbiota,reducing damage to the intestinal barrier,and improving the efficiency of nutrient utilization to alleviate the adverse effects caused by the decrease in dietary energy level.展开更多
文摘AIM: To study the modulation of glutamate on post-ischemic intestinal and cerebral inflammatory responses in a ischemic and excitotoxic rat model.METHODS: Adult male rats were subjected to bilateral carotid artery occlusion for 15 min and injection of monosodium glutamate intraperitoneally, to decapitate them at selected time points. Tumor necrosis factor alpha (TNF-α) level and nuclear factor kappa B (NF-κB) activity were determined by enzyme-linked immunosorbant assay (ELISA) and electrophoretic mobility shift assay (EMSA), respectively.Hemodynamic parameters were monitored continuously during the whole process of cerebral ischemia and reperfusion.RESULTS: Monosodium glutamate (MSG) treated rats displayed statistically significant high levels of TNF-α in cerebral and intestinal tissuess within the first 6 h of ischemia. The rats with cerebral ischemia showed a minor decrease of TNF-α production in cerebral and intestinal tissuess. The rats with cerebral ischemia and treated with MSG displayed statistically significant low levels of TNF-α in cerebral and intestinal tissues. These results correlated significantly with NF-κB production calculated at the same intervals. During experiment, the mean blood pressure and heart rates in all groups were stable.CONCLUSION: Glutamate is involved in the mechanism of intestinal and cerebral inflammation responses. The effects of glutamate on cerebral and intestinal inflammatory responses after ischemia are up-regulated at the transcriptional level,through the NF-κB signal transduction pathway.
基金financially supported by the China Agriculture Research System Program(CARS-41-G11)
文摘This experiment aimed to discuss and reveal the effect and mechanism of mannanase on intestinal inflammation in broilers triggered by a soybean meal diet.In this experiment,384 Arbor Acres broilers at1 d old were randomly divided into 3 treatment groups.The broilers were fed a corn-soybean meal basal diet,a low-energy diet(metabolizable energy reduced by 50 kcal/kg),and a low-energy diet supplemented with 100 mg/kg mannanase for 42 d.The low-energy diet increased feed conversion ratio from0 to 42 d,reduced ileal villus height and villus height-to-crypt depth ratio and upregulated the expression of nuclear factor kappa B(NF-κB)in the ileum(P<0.05).It also reduced cecal short-chain fatty acids(SCFA),such as acetic acid(P<0.05).Compared with low-energy diets,the addition of mannanase increased body weight at 42 d,promoted the digestibility of nutrients,and maintained the morphology and integrity of the intestinal epithelium of broilers(P<0.05).In addition,mannanase upregulated the expression of claudin-1(CLDN1)and zonula occludens-1(ZO-1)in the jejunum at 21 d,downregulated the expression of ileal NF-κB,and increased the content of isobutyric acid in the cecum of broilers(P<0.05).The results for the ileal microbiota showed that a low-energy diet led to a decrease in the relative abundance of Lactobacillus reuteri in the ileum of broilers.The addition of mannanase increased the relative abundance of Lactobacillus-KC45b and Lactobacillus johnsonii in broilers.Furthermore,a low-energy diet reduced the relative abundance of Butyricicoccus in the intestine of broilers and inhibited oxidative phosphorylation and phosphoinositol metabolism.Mannanase increased the relative abundance of Odoribacter,promoted energy metabolism and N-glycan biosynthesis,and increased the activities of GH3 and GH18.It is concluded that mannanase could improve the growth performance of broilers by reducing the expression of NF-κB in the ileum,increasing the production of SCFA in the cecum,suppressing intestinal inflammation,balancing the intestinal microbiota,reducing damage to the intestinal barrier,and improving the efficiency of nutrient utilization to alleviate the adverse effects caused by the decrease in dietary energy level.