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Publications (2)1.81 Total impact

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    ABSTRACT: Macrophage plays a vital role in sepsis. However, the modulatory effect of glutamine (Gln) on macrophage/ monocyte-mediate cytokines release is still controversial. Thus, we investigated the effect of Gln on macrophage tumor necrosis factor (TNF)-alpha release and heat shock protein (HSP) 72 expression in vivo and in vitro. Data from our study indicated that the increase of HSP72 expression was significant at 8 mM of Gln 4 h after lipopolysaccharide (LPS) stimulation and became independent of Gln concentrations at 24 h, whereas TNF-alpha release was dose- and time-dependent on Gln. Heat stress (HS) induced more HSP72 and less TNF-alpha production compared with the non-HS group. However, the production of TNF-alpha in cells pretreated with HS was increased with increasing concentrations of Gln. Treatment with various concentrations of Gln for 1 h and then 0.5 mM Gln for 4 h led to an increase in HSP72 expression, but not in TNF-alpha production. In sepsis model mice, Gln treatment led to a significantly lower intracellular TNF-alphalevel and an increase in HSP72 expression in mouse peritoneal macrophages. Our results demonstrate that Gln directly increases TNF-alpha release of LPS-stimulated RAW264.7 macrophages in a dose-dependent manner, and also decreases mouse peritoneal macrophages TNF-a release in the sepsis model. Taken together, our data suggest that there may be more additional pathways by which Gln modulates cytokine production besides HSP72 expression in macrophage during sepsis.
    Acta Biochimica et Biophysica Sinica 03/2009; 41(2):171-7. · 1.81 Impact Factor
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    ABSTRACT: To evaluate the effects of glutamine (Gln) on macrophages cytokines release and heat shock protein 72 (HSP72) expression in vivo and in vitro, and explore the anti-inflammation mechanisms of Gln during sepsis. In experiment one, mouse peritoneal macrophage cell line RAW264.7 cells were divided into 0, 0.5 and 8 mmol/L Gln groups, and cells and supernatants were harvested at 0, 1, 4, 12 and 24 hours after lipopolysaccharide (LPS) challenge. In experiment two, forty-five Kunming mice were randomized into sham-operation group (Sham), sepsis model group, and Gln group. Sepsis was induced by cecal ligation and puncture (CLP). Either Gln 0.75 g/kg (Gln group) or saline (Sham and model group) was administered immediately after CLP via tail-vein injection. Blood sample was collected at 6 hours, and macrophages were harvested by peritoneal lavage. Tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and IL-10 contents in supernatant, serum and cell lysate were analyzed with enzyme-linked immunosorbent assay (ELISA), macrophages HSP72 expression was assessed with Western blotting. Gln promoted RAW264.7 cells to release TNF-alpha, IL-6 and IL-10 in a dose-dependent and time-dependent manner in vitro (P<0.05 or P<0.01), and significantly increased HSP72 expression in 8 mmol/L Gln group at 4 hours after LPS stimulation (both P<0.01). In vivo, in animals given Gln intracellular TNF-alpha and IL-6 levels were significantly lower than sepsis animals (P<0.01 and P<0.05), but there was no statistically significant difference in intracellular IL-10 levels among three groups. The serum levels of TNF-alpha in Gln group were significantly lower than in model group (P<0.05), while serum IL-6 and IL-10 levels were similar between two groups. Gln treatment led to significant HSP72 expression compared to model and Sham groups (both P<0.01). Gln can promote inflammatory cytokines release from macrophages in vitro, which cannot be attenuated by HSP72 expression induced by Gln in LPS challenged RAW264.7 macrophages. Gln treatment significantly decreases intracellular TNF-alpha and IL-6 levels in vivo during sepsis. HSP72 expression increases after Gln treatment both in vivo and in vitro. These data implicate that HSP72 may not play a major role in attenuating the inflammatory response after Gln administration in sepsis.
    Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 08/2008; 20(8):456-60.