Prevention of bacterial translocation using beta-(1-3)-D-glucan in small bowel ischemia and reperfusion in rats

Prevention of bacterial translocation using beta-(1-3)-D-glucan in small bowel ischemia and reperfusion in rats
复制标题

DOI:
10.1590/s0102-86502006001000005
复制
发表时间:
2006-01-01
影响因子:
1.1
通讯作者:
Medeiros, Aldo Cunha
Medeiros, Aldo Cunha
中科院分区:
医学4区
文献类型:
--
作者:
Araújo-Filho, Irami;Rêgo, Amália Cínthia Meneses;Medeiros, Aldo Cunha

文献摘要

被引文献

相似文献

目的:研究β -(1 - 3)- D - 葡聚糖在小肠缺血/再灌注损伤大鼠中对⁹⁹ᵐTc标记的大肠杆菌易位和细胞因子分泌的作用。 方法:将五组(每组n = 10)Wistar大鼠分为对照组(C)、假手术组(S)、肠缺血45分钟/再灌注60分钟组(IR)以及肠缺血45分钟/再灌注60分钟且肌肉注射2mg/Kg葡聚糖组(I/R + 葡聚糖)。采用放射性计数和菌落形成单位/克(CFU/g)测定标记细菌向肠系膜淋巴结、肝脏、脾脏、肺和血清的易位情况。通过酶联免疫吸附测定(ELISA)检测血清肿瘤坏死因子α(TNFα)、白细胞介素 - 1β(IL - 1β)、白细胞介素 - 6(IL - 6)和白细胞介素 - 10(IL - 10)。 结果:IR组的CFU/g和放射性计数高于I/R + 葡聚糖组大鼠。在C组、S组和S + 葡聚糖组中,很少检测到细菌和放射性计数。与未治疗的IR组动物相比,I/R + 葡聚糖组大鼠的IL - 10升高,血清TNFα、IL - 1β和IL - 6的产生受到抑制。 结论:β -(1 - 3)- D - 葡聚糖在肠缺血/再灌注过程中调节促炎和抗炎细胞因子的产生,并减弱标记细菌的易位。
PURPOSE: To investigate the role of beta-(1-3)-D-glucan on 99mTc labelled Escherichia coli translocation and cytokines secretion in rats submitted to small bowel ischemia/reperfusion injury.METHODS: Five groups (n=10 each) of Wistar rats were subjected to control(C), sham(S), group IR subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R), and group I/R+glucan subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R) and injected with 2 mg/Kg intramuscular. Translocation of labelled bacteria to mesenteric lymph nodes, liver, spleen, lung and serum was determined using radioactivity/count and colony forming units/g(CFU/g). Serum TNFalpha, IL-1beta, IL-6, IL-10 were measured by ELISA.RESULTS: CFU/g and radioactivity/count were higher in I/R than in I/R+glucan rats. In C, S and S+glucan groups, bacteria and radioactivity/count were rarely detected. The I/R+glucan rats had enhancement of IL-10 and suppressed production of serum TNFalpha, IL-1beta and, IL-6, compared to I/R untreated animals.CONCLUSION: The beta-(1-3)-D-glucan modulated the production of pro-inflammatory and anti-inflammatory cytokines during bowel ischemia/reperfusion, and attenuated translocation of labelled bacteria.