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Objectives:To investigate the intestinal microflora status related to ischemia/reperfusion(I/R)liver injury and explorethe possible mechanism.Methods:Specific pathogen free grade Sprague-Dawley rats were randomized into three groups:Controlgroup(n=8),sham group(n=6)and I/R group(n=10).Rats in the control group did not receive any treatment,rats in the I/R groupwere subjected to 20 min of liver ischemia,and rats in the sham group were only subjected to sham operation.Twenty-two hourslater,the rats were sacrificed and liver enzymes and malondialdehyde(MDA),superoxide dismutase(SOD),serum endotoxin,intestinal bacterial counts,intestinal mucosal histology,bacterial translocation to mesenteric lymph nodes,liver,spleen,andkidney were studied.Results:Ischemia/reperfusion increased liver enzymes,MDA,decreased SOD,and was associated withplasma endotoxin elevation in the I/R group campared to those in the sham group.Intestinal Bifidobacteria and Lactobacillidecreased and intestinal Enterobacterium and Enterococcus
Objectives: To investigate the intestinal microflora status related to ischemia / reperfusion (I / R) liver injury and explore the possible mechanism. Methods: Specific pathogen free grade Sprague-Dawley rats were randomized into three groups: Controlgroup (n = 8) (n = 6) and I / R group (n = 10). Rats in the control group did not receive any treatment, rats in the I / R groupwere subjected to 20 min of liver ischemia, and rats in the sham group were only The rats were sacrificed and liver enzymes and malondialdehyde (MDA), superoxide dismutase (SOD), serum endotoxin, intestinal bacterial counts, intestinal mucosal histology, bacterial translocation to mesenteric lymph nodes, liver, spleen , andkidney were studied.Results: Ischemia / reperfusion increased liver enzymes, MDA, decreased SOD, and was associated withplasma endotoxin elevation in the I / R group campared to those in the sham group.Intestinal Bifidobacteria and Lactobacilliideased and intestinal Enterobacteri um and Enterococcus