Children Nutrition Research Center
Children Nutrition Research Center
Shiyu S.,Chongqing Medical University |
Zhiyu L.,Chongqing Medical University |
Mao Y.,Chongqing Medical University |
Lin B.,Chongqing Medical University |
And 4 more authors.
BMC Cell Biology | Year: 2011
Background: Lung injury induced by lipopolysaccharide (LPS) remains one of the leading causes of morbidity and mortality in children. The damage to membrane phospholipids leads to the collapse of the bronchial alveolar epithelial barrier during acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Phospholipase A2(PLA2), a key enzyme in the hydrolysis of membrane phospholipids, plays an important traumatic role in pulmonary inflammation, and Clara cell secretory protein (CCSP) is an endogenous inhibitor of PLA2. Our previous study showed that polydatin (PD), a monocrystalline extracted from a traditional Chinese medicinal herb (Polygonum cuspidatum Sieb, et Zucc), reduced PLA2activity and sPLA2-IIA mRNA expression and mitigated LPS-induced lung injury. However, the potential mechanism for these effects has not been well defined. We have continued to investigate the effect of PD on LPS-induced expression of CCSP mRNA and protein in vivo and in vitro.Results: Our results suggested that the CCSP mRNA level was consistent with its protein expression. CCSP expression was decreased in lung after LPS challenge. In contrast, PD markedly increased CCSP expression in a concentration-dependent manner. In particular, CCSP expression in PD-pretreated rat lung was higher than in rats receiving only PD treatment.Conclusion: These results indicated that up-regulation of CCSP expression causing inhibition of PLA2activation may be one of the crucial protective mechanisms of PD in LPS-induced lung injury. © 2011 Shiyu et al; licensee BioMed Central Ltd.
Liu X.,Children Nutrition Research Center |
Liu X.,Chongqing Medical University |
Li Y.,Children Nutrition Research Center |
Li Y.,Chongqing Medical University |
And 13 more authors.
Nutrition | Year: 2014
Objectives: Vitamin A (VA) is a critical micronutrient for life, especially during growth and development. There is a close relationship between VA deficiency (VAD) and the morbidity of diarrhea in the clinical setting. However, the regulatory mechanisms of VA are not clearly understood. Methods: Specific-pathogen-free Wistar rats received a diet with or without VA before gestation. The offspring were submitted to an abdominal injection of Escherichia coli lipopolysaccharide. After the challenge, which lasted for 12 h, the serum retinol was detected by high-performance liquid chromatography, and the level of immunoglobulin A in the stool was analyzed by enzyme-linked immunosorbent assay. The lymphocyte immunophenotypes were evaluated with the use of flow cytometry with samples collected from the spleen, the mesenteric lymph nodes, Peyer patches, and intestinal intraepithelial lymphocytes. Results: Early life VAD, independent of the lipopolysaccharide challenge, significantly decreased serum retinol level and CD8+ intestinal intraepithelial lymphocytes. The level of immunoglobulin A secretion and percentages of splenic CD4+CD8+ T cells were affected by the interaction effects of the lipopolysaccharide challenge and VAD treatment. Gestational VAD significantly increased the percentages of B cells in the mesenteric lymph nodes and decreased the percentages of CD11 C+ dendritic cells and CD4+CD25+ T cells from the Peyer patches. The lipopolysaccharide challenge only significantly increased percentages of splenic CD4+CD25+ T cells. The intestinal tissue of the pups with VAD displayed mild inflammation. Conclusions: Gestational or early life VAD decreases the numbers of immune cells in offspring, which may partly suppress the activities of the mucosal immune responses in the intestine. This suggests that more attention should be given to the VA nutritional state of children and women of reproductive age. © 2014 Elsevier Inc.
He J.,Children Nutrition Research Center |
He J.,Chongqing Medical University |
Li T.,Children Nutrition Research Center |
Li T.,Chongqing Medical University |
And 8 more authors.
Clinical Biochemistry | Year: 2016
Objectives: Oxidative stress (OS) may play a critical role in cell aging and neurologic disorders that are often seen in Down syndrome (DS) patients. The aim of this study was to determine the antioxidant enzyme level and lipoperoxidation status in blood from DS children. Design and methods: In a cross-sectional study, we recruited a total of 36 DS children and 40 healthy controls (HCs). All subjects were free of infection according to the C reactive protein (CRP) value and routine peripheral blood profile. The activities of total superoxide dismutases (SODs), extracellular glutathione peroxidase (GPx3),malondialdehyde (MDA) and nitric oxide synthase (NOS) concentrations in peripheral blood were measured by spectrophotometric methods. The relationship of SOD and GPx3 was analyzed in the two groups. Results: The two groups were similar with respect to age, gender and peripheral blood profiles. The total SOD activity was significantly increased, while the GPx3 activity was significantly reduced in the DS group compared to the HCs ( p= 0.000, p= 0.033 respectively). The MDA level was higher in DS children (p= 0.013). There was no significant difference in NOS between DS and HCs ( p= 0.708). A significant negative correlation between GPx3 and SOD activity was identified in DS ( r= 0.14, p= 0.018) but not in the HC group. Conclusions: Abnormal redox metabolism takes place in DS individuals. Reducing GPx3 may be a compensatory mechanism of protection against intracellular OS. Moreover, monitoring of decreases in GPx3 activity may be a useful biomarker for evaluating OS in DS patients. © 2015 The Canadian Society of Clinical Chemists.