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Objective To investigate the effects of N-acetyl-D-glucosamine(GlcNAc)on acute pancreatitis in rats.Methods Twenty male SD rats were randomly divided into a control group,AP group,low GlcNAc + AP group and high GlcNAc + AP group,with five rats in each group.Acute pancreatitis was induced in AP group,low GlcNAc + AP group and high GlcNAc + AP group by two intraperitoneal injections of 2.5 g/kg L-arginine with a 1 hour interval.Among them,low GlcNAc + AP group and high GlcNAc + AP group were administered 50 and 200 mg/kg GlcNAc,respectively,by intraperitoneal injection at 24 hours before the first intraperitoneal injection of L-arginine.Group control and AP were intraperitoneally injected with the same volume of normal saline.After 24 h,the rats were sacrificed,and serum and pancreatic tissues were collected.Pancreatic tissue morphology was observed by HE staining,and serum levels of amylase(AMY),lipase(LPS),interleukin-1β(IL-1β),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),superoxide dismutase(SOD)and malondialdehyde(MDA)were measured by enzyme-linked immunosorbent assay.Protein expression of nuclear factor E2-related factor 2(NRF2),heme oxygenase-1(HO-1),and peroxisome proliferator-activated receptor-γ(PPAR-γ)in pancreatic tissue was detected by Western Blot.Cluster of differentiation(CD)86,CD206 and macrophage markers(F4/80)were detected by immunofluorescence.Expression of CD86 and CD206 in pancreatic tissue was detected by immunohistochemistry.Results(1)Compared with control group,AMY,LPS,IL-1β,IL-6,TNF-α,and MDA levels and pancreatic CD86 expression in AP group were significantly increased(P<0.05),while SOD activity,protein expression levels of NRF2,HO-1,and PPAR-γ,and pancreatic CD206 expression were significantly decreased(P<0.05).(2)Compared with AP group,serum IL-1β,IL-6,TNF-α,MDA,and LPS and the pancreatic CD86 expression in low GlcNAc + AP group were significantly decreased(P<0.05).The PPAR-γ protein level in the pancreas was significantly increased(P<0.05).(3)Compared with AP group,serum AMY,LPS,IL-1β,IL-6,TNF-α,and MDA and pancreatic CD86 expression in high GlcNAc + AP group were significantly decreased(P<0.05),while serum SOD,and NRF2,HO-1,PPAR-γ,and pancreatic CD206 expression were significantly increased(P<0.05).(4)Compared with low GlcNAc + AP group,serum LPS,IL-1β and IL-6 in high GlcNAc + AP group were significantly decreased(P<0.05).Pancreatic expression of HO-1,PPAR-γ,and pancreatic CD206 were significantly increased(P<0.05).Conclusion GlcNAc treatment attenuates acute pancreatitis injury in AP rats,possibly by activating the NRF2/HO-1 signaling pathway to inhibit oxidative stress and promoting M2 macrophage polarization to attenuate pancreatic injury in AP rats.
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A new chitin-binding lectin was purified from a Bangladeshi cultivar ‘Deshi’ of potato (Solanum tuberosum L.) through anion-exchange and affinity chromatographies using a chitin column. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) showed the molecular mass of the lectin as 20,000 Daltons. This molecular mass was almost half of the molecular masses of chitin-binding lectins derived from other potatoes. The lectin showed both bactericidal and growth-inhibiting activities against Gram-positive (Listeria monocytogenes) and Gram-negative (Escherichia coli, Salmonella enteritidis and Shigella boydii) pathogenic bacteria. It also showed antifungal activity against Rhizopus spp., Penicillium spp. and Aspergillus niger. Biofilm produced by the bacterium Pseudomonas aeruginosa was dose-dependently reduced by 5-20% in 24 h after administration of the lectin, which was attributed to the glycan-binding property of the lectin having affinity to GlcNAc polymers. It was the first observation that any potato lectin prevented biofilm formation by P. aeruginosa and, therefore, could have possible applications in clinical microbiology and biomedical science.
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Antibacterianos/farmacologia , Bactérias/efeitos dos fármacos , Biofilmes/efeitos dos fármacos , /metabolismo , Lectinas de Plantas/isolamento & purificação , Lectinas de Plantas/farmacologia , Pseudomonas aeruginosa/efeitos dos fármacos , Pseudomonas aeruginosa/crescimento & desenvolvimento , Solanum tuberosum/classificação , Solanum tuberosum/crescimento & desenvolvimento , Solanum tuberosum/metabolismoRESUMO
Lectin-carbohydrate binding may be involved in the recognition of Schistosoma mansoni sporocysts by haemocytes of Biomphalaria; therefore, we tested if this interaction is associated with snail resistance against Schistosoma infection. In vitro data showed that most of the S. mansoni sporocysts cultured with haemocytes from Biomphalaria glabrata BH, a highly susceptible snail strain, had a low number of cells that adhered to their tegument and a low mortality rate. Moreover, the addition of N-acetyl-D-glucosamine (GlcNAc) did not alter this pattern of adherence and mortality. Using haemocytes and haemolymph of Biomphalaria tenagophila Cabo Frio, we observed a high percentage of sporocysts with adherent cells, but complete encapsulation was not detected. Low concentrations of GlcNAc increased haemocyte binding to the sporocysts and mortality, which returned to basal levels with high concentrations of the carbohydrate. In contrast, haemocytes plus haemolymph from B. tenagophila Taim encapsulated cellular adhesion index of level 3 and destroyed over 30 percent of the S. mansoni sporocysts in culture. Interestingly, the addition of GlcNAc, but not mannose, to the culture medium resulted in the significant inhibition of cellular adhesion to the parasite tegument and the reduction of parasite mortality, suggesting that GlcNAc carbohydrate moieties are important to the recognition of S. mansoni by B. tenagophila Taim.
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Animais , Acetilglucosamina/imunologia , Biomphalaria/parasitologia , Hemócitos/parasitologia , Hemolinfa/parasitologia , Oocistos/fisiologia , Schistosoma mansoni/imunologia , Biomphalaria/citologia , Carboidratos/imunologia , Interações Hospedeiro-ParasitaRESUMO
Objective To evaluate the efficacy and safety of N-acetyl-D-glucosamine in treatment of diarrhea-predominant irritable bowel syndrome (D-IBS). Methods A multi-center, randomized, double-blind, placebo-controlled clinical study was performed in 430 patientswith D-IBS. After 2-week baseline period, eligible subjects were randomly either received 100 mg of N-acetyl-D-glucosamine (treated group,n=323) or placebo (control group,n= 107) 3 times a day for consecutive 4 weeks, followed by 2-week withdrawal follow-up. The major parameters were assessed by visual analogue scale (VAS) score and Common Symptom Sensation score. The minor parameters included abdominal pain or discomfort, severity of diarrhea, bloating, urgency, defecation frequencies with consistency per bowel movement which was judged by bristol stool scale and utilization of Smect. The evidence of adverse events was reeoded. Results The major parameters were singnifieantly improved in the treated group with effective rate of 65.16 % at the fourth week of treatment in comparison with control group (effective rate of 34. 29% ,P<0.01). Except the utilization of Smect (P= 1.00), the other minor parameters were significantly improved in treated group compared with control group (P< 0.01) after 1 week treatment. The occurrence of adverse events was 0.96% in the treated group and 0. 95% in the control group (P = 1. 00). Conclusions The results indicate that N-acetyl-D-glucosamine is effective and safe in the treatment of D-IBS by improving ecological environment and preventing activation of mast cells.
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Objective To investigate the regulative role of N-Acetyl-D-glucosamine(GlcNAc) on the stressed mice macrophages function.Methods The stressed mice model was established by electric footshock method.The mice were divided into 5 groups:normal control group,stressed mice model group,low dose Glc-NAc treatment group(0.25 ml 15% GlcNAc),medium-dose GlcNAc treatment group(0.5 ml 15% GlcNAc) and high-dose GlcNAc treatment group(1 ml 15% GlcNAc).GlcNAc was intragastrically injected to corresponding mice 2 h before the electrical stimulation.Peritoneal macrophage(PM?) phagocytosis capability was detected by phagocytosis saccharomycete assay,and PM? energy metabolism was detected by MTT assay.Results Compared with normal control group,stressed mice PM? phagocytosis capability was significantly lower(P
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We use chitosan and n -acetyl -d -glucosamine to inhibit fibroblast proliferation which was cultured in vitro. The result shows that n - acetyl - d - glucosamine: ID50=16. 35mg/L, chitosan: ID50=69. 59mg/L. We also plant the chitosan membrane to the rabbit body to test its bio-degradation. The result shows that the molecular weight of chitosan drops 17% and 6% after 25 days and 18 days, respectively. On the basis of these results, we have obtained a conclusion that we can probably use chitosan to continuously release n-acetyl -d-glucosamine which can inhibit fibroblast proliferation effectively.