Shan Wang

Publications (3)17.23 Total impact

• Article: Endotoxin tolerance of adrenal gland: attenuation of corticosterone production in response to lipopolysaccharide and adrenocorticotropic hormone.

  Shujuan Liu, Xiaoyan Zhu, Yujian Liu, Changnan Wang, Shan Wang, Xiaolu Tang, Xin Ni
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  ABSTRACT: Reversible adrenal insufficiency frequently has been diagnosed in critically ill patients with sepsis who have either low basal cortisol levels or low cortisol responses to adrenocorticotropic hormone (ACTH) stimulation. It is generally accepted that a phenomenon called "endotoxin tolerance" contributes to immunosuppression during sepsis. The present study was to investigate whether endotoxin tolerance occurs in the adrenal gland, leading to hyporesponsiveness of adrenal gland during sepsis. Controlled laboratory experiment. University research laboratory. Sprague-Dawley male rats 200-250 g and primary isolated adrenal fasciculata-reticularis cells. Rats received intra-arterial injection of purified lipopolysaccharide (0.5 mg/kg) through indwelling femoral arterial catheters, and 24 hrs later the adrenocortical sensitivity to exogenous ACTH (10 ng/kg) was detected. Primary fasciculata-reticularis cells were pretreated with lipopolysaccharide at 0.1-100 ng/mL or with ACTH at 0.01-10 ng/mL and then challenged, in fresh media, with 1 μg/mL lipopolysaccharide or 10 ng/mL ACTH. Toll-like receptor 4 was expressed in adrenal gland and primary fasciculata-reticularis cells. Plasma corticosterone response to ACTH was decreased in rats receiving preinjection of lipopolysaccharide. Lipopolysaccharide pretreatment caused a significant decrease in corticosterone production in response to subsequent ACTH and lipopolysaccharide stimulation in primary fasciculata-reticularis cells. Lipopolysaccharide pretreatment inhibited ACTH- and lipopolysaccharide-induced expression of steroid metabolizing enzymes. Lipopolysaccharide significantly decreased Toll-like receptor 4 and ACTH receptor expression. Pre-exposure to lipopolysaccharide resulted in hyporesponsiveness to ACTH stimulation in rats. In vitro, lipopolysaccharide pretreatment impaired corticosterone production of fasciculata-reticularis cells in response to ACTH and lipopolysaccharide, which was associated with decreased expression of synthetic enzymes required for corticosterone production. Our results indicate that endotoxin tolerance of adrenal gland is one of the mechanisms for adrenocortical insufficiency during sepsis.
  Critical care medicine 03/2011; 39(3):518-26. · 6.37 Impact Factor
• Article: Isoflavones suppress cyclic adenosine 3',5'-monophosphate regulatory element-mediated transcription in osteoblastic cell line.

  Xiaolu Tang, Xiaoyan Zhu, Shujuan Liu, Shan Wang, Xin Ni
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  ABSTRACT: Soy isoflavones have been implicated to exert benefit on bone loss in postmenopausal women. Isoflavones can induce estrogen response element-mediated transcription in osteoblastic cells. In the present study, we investigate whether isoflavones genistein and daidzein regulate target gene transcription through cAMP regulatory element (CRE) in osteoblastic cells. It was found that 17β-estradiol (E(2)), genistein and daidzein suppressed the transcriptional activity of CRE-luciferase reporter gene in human osteoblastic cell line MG-63 cells. E(2) and genistein but not daidzein inhibited the cAMP analogue 8-Br cAMP-induced transcription of CRE reporter gene. Both genistein and E(2) inhibited basal and cAMP-induced mRNA levels of endogenous estrogen responsive genes containing CRE/CRE-like elements in their promoter regions, including interleukin (IL) 8 and serum- and glucocorticoid-inducible kinase 1 (SGK1). Daidzein inhibited basal and cAMP-induced IL-8, but not SGK1 mRNA expression. The inhibitory effects of E(2), genistein and daidzein on CRE-mediated transcription activity were enhanced by estrogen receptor (ER) α overexpression in MG-63 cells, which could be blocked by nonselective ER antagonists ICI182780, 4-OH tamoxifen and specific ERα antagonist MPP. Genistein and daidzein, but not E(2) treatment, caused a significant decrease in CRE-mediated transcription activity in ERβ-transfected MG-63 cells, which could be blocked by ICI182780, 4-OH tamoxifen and the selective ERβ antagonist (R,R)-5,11-diethyl-5.6,11,12-tetradro-2,8-chrysenediol. Our results indicate that isoflavones genistein and daidzein might modulate bone remodeling through ERs by regulating target gene expression through the CRE motifs.
  The Journal of nutritional biochemistry 11/2010; 22(9):865-73. · 4.29 Impact Factor
• Article: Glucocorticoids suppress cystathionine gamma-lyase expression and H2S production in lipopolysaccharide-treated macrophages.

  Xiao-Yan Zhu, Shu-Juan Liu, Yu-Jian Liu, Shan Wang, Xin Ni
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  ABSTRACT: Hydrogen sulfide (H(2)S) plays an important role in inflammation. We showed that macrophages expressed the H(2)S-forming enzyme cystathionine gamma-lyase (CSE) and produced H(2)S. Lipopolysaccharide (LPS) stimulated the CSE expression and H(2)S production rate. l-cysteine reduced LPS-induced nitric oxide (NO) production. CSE inhibitor blocked the inhibitory effect of l-cysteine. CSE knockdown increased, whereas CSE overexpression decreased LPS-induced NO production. Dexamethasone suppressed LPS-induced CSE expression and the H(2)S production rate as well as NO production. l-arginine increased, whereas N(G)-nitro-l-arginine methyl ester (l-NAME) decreased LPS-induced CSE expression and H(2)S production. Dexamethasone plus l-NAME significantly decreased LPS-induced CSE expression and H(2)S production compared to l-NAME. Our results suggest that macrophages are one of the H(2)S producing sources. H(2)S might exert anti-inflammatory effects by inhibiting NO production. Dexamethasone may directly inhibit CSE expression and H(2)S production, besides the NO-dependent way. Inhibition of H(2)S and NO production may be a mechanism by which glucocorticoids coordinate the balance between pro- and anti-inflammatory mediators during inflammation.
  Cellular and Molecular Life Sciences CMLS 04/2010; 67(7):1119-32. · 6.57 Impact Factor