NF-κB levels in the liver of young rats with endotoxemic liver injury / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study hepatic NF-κB level following endotoxemic liver injury, and its relationship with hepatic TNF-α and IL-6 levels in young rats.</p><p><b>METHODS</b>Forty 18-day-old rats were randomly assigned to a normal control and an endotoxemia group. Endotoxemia was induced by lipopolysaccharide injection (LPS, 5 mg/kg). The endotoxemia group was subdivided into four groups sampled at 2, 6, 12 and 24 hrs after LPS injection (n=8 each). Pathological changes in liver cells were observed under a light microscope. TNF-α and IL-6 levels in liver tissue homogenates were measured using ELISA. Reitman-Frankel was used to measure serum ALT concentrations. NF-κB activation level in liver tissues was detected by immunohistochemistry.</p><p><b>RESULTS</b>Liver tissue injury was the most obvious 6 hrs after LPS injection under the light microscope, and the damage rating of liver tissues was significantly higher in the endotoxemia group than that in the normal control group at all time points (P<0.05). ALT levels in the endotoxemia group were significantly higher than those in the normal control group 6, 12 and 24 hrs after LPS injection (P<0.05). NF-κB p65 protein expression in liver cells (percentage of nuclear positive cells) in the endotoxemia groups was significantly higher than that in the normal control group (P<0.05). TNF-α and IL-6 levels in liver tissue homogenates in the endotoxemia groups were significantly higher than those in the normal control group 6 and 12 hrs after LPS injection (P<0.05).</p><p><b>CONCLUSIONS</b>Endotoxemia can cause liver injury, resulting in liver cell damage and changes in liver function. NF-κB activation is involved in endotoxemic liver injury which may be mediated by inflammatory cytokines TNF-α and IL-6 synthesis.</p>

Effect of oral glutamine on intestinal barrier function in young rats with endotoxemia / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the effect of glutamine on intestinal barrier function by examining the changes of plasma D-lactic levels and diamine oxidase (DAO) levels in plasma and intestinal tissue after glutamine intervention in young rats with endotoxemia.</p><p><b>METHODS</b>Eighty 18-day-old rats were randomly divided into endotoxemia and glutamine intervention groups (n=40 each). Endotoxemia was induced by lipopolysaccharide (LPS) injection. Plasma and small intestine homogenate were collected 1.5, 6, 24 and 72 hrs and 7 days after LPS injection. The glutamine intervention group was immediately administered with oral glutamine (2 g/kg) after LPS injection. Afterwards, glutamine was administered once daily. Plasma D-lactic and DAO levels and intestinal DAO levels were measured.</p><p><b>RESULTS</b>Plasma DAO activity in the glutamine intervention group was significantly lower than that in the endotoxemia group 6 and 72 hrs after LPS injection (P<0.05). In contrast, the intestinal DAO activity in the glutamine intervention group was significantly higher than that in the endotoxemia group 6, 24 and 72 hrs and 7 days after LPS injection (P<0.05 or 0.01). Plasma D-lactic levels in the glutamine intervention group were significantly lower than those in the endotoxemia group 6, 24 and 72 hrs and 7 days after LPS injection (P<0.01).</p><p><b>CONCLUSIONS</b>Glutamine may reduce the permeability of intestinal mucosa, and thus provides protective effects on intestinal barrier function in rats with endotoxemia.</p>

Relationship between gene polymorphisms in MMP-9 and Helicobacter pylori-related upper gastrointestinal disease in children / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the relationship of the promoter of matrix metalloproteinase-9 (MMP-9) gene polymorphisms with the susceptibility and clinical features of Helicobacter pylori (H. pylori)-related chronic gastritis and duodenal ulcer in children.</p><p><b>METHODS</b>One hundred children with chronic gastritis, 32 children with duodenal ulcer and 102 healthy children were enrolled.The promoter of MMP-9-1562C/T gene polymorphisms were genotyped by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) and sequencing. MMP-9 mRNA expression in gastric mucosa was confirmed by reverse transcription polymerase chain reaction.</p><p><b>RESULTS</b>The genotype distributions and allele frequencies of MMP-9-1562C/T gene polymorphisms were similar in gastric upper gastrointestinal disease and healthy subjects. The relative risk for H.pylori infection in C/C genetype carriers was 3.1 times as high as that in T allele (C/T+T/T) carriers in children with chronic gastritis. MMP-9-1562 C/T gene polymorphisms did not affect MMP-9 mRNA expression level.</p><p><b>CONCLUSIONS</b>These data suggest that MMP-9-1562 C/T gene polymorphisms are not associated with susceptibility to chronic gastritis and duodenal ulcer in children. The C/C genotype of MMP-9-1562 C/T gene polymorphism might be associated with H.pylori infection.</p>