Glucocorticoid Modulates High-Mobility Group Box 1 Expression and Toll-Like Receptor Activation in Obstructive Jaundice

Huang, Ying‐Hsien; Wang, Pei‐Wen; Tiao, Mao‐Meng; Chou, Ming-Huei; Du, Yung-Ying; Huang, Chao‐Cheng; Chuang, Jiin‐Haur

doi:10.1016/j.jss.2011.05.033

Cited by 18 publications

(9 citation statements)

References 43 publications

(51 reference statements)

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“…In addition, BDL in the control group significantly upregulated the mRNA expression levels of TLR-4 and TLR-9 (P<0.05; Fig. 5) compared with the sham group, which is consistent with previous studies (4). In the present study it was demonstrated that histone preconditioning significantly ameliorated the upregulation of the mRNA expression levels of TLR-4 and TLR-9.…”

Section: Resultssupporting

confidence: 91%

“…One of the major consequences of OJ is the development of severe liver injury (2). The mechanisms responsible for the pathogenesis of OJ-induced liver injury remain largely unknown, although inflammatory cell infiltration, microvascular perfusion failure and Toll-like receptor (TLR) activation are reported to be involved (3,4). At present, there are no effective treatments to protect against OJ-induced liver injury, thus, novel therapeutic strategies are urgently required.…”

Section: Introductionmentioning

confidence: 99%

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Histone preconditioning protects against obstructive jaundice-induced liver injury in rats

Zhou¹,

Ni²,

Liu³

et al. 2014

Experimental and Therapeutic Medicine

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A major consequence of obstructive jaundice (OJ) in clinical practice is the development of severe liver injury, and at present, no effective treatments have been developed to protect against it. Preconditioning with damage-associated molecular pattern (DAMP) molecules has been demonstrated to protect multiple organs from injury, and histones have been recently identified as DAMP molecules. The aim of the present study was to investigate the protective effect of histone preconditioning against OJ-induced liver injury in rats and the involvement of Toll-like receptors. Rats were administered histone proteins (200 μg/kg; 1 ml) or physiological saline (1 ml) intraperitoneally 24 h prior to being subjected to bile duct ligation (BDL). The serum levels of liver enzymes and bilirubin, as well as the histopathology were analyzed. The mRNA expression of interleukin-6 (IL-6) in the liver tissue was analyzed using quantitative polymerase chain reaction. BDL in the control group caused severe OJ-induced liver injury, as indicated by the significantly elevated levels of liver enzymes and mRNA levels of IL-6, and confirmed by histopathological alterations. However, histone preconditioning significantly ameliorated the OJ-induced liver injury caused by BDL, as shown by an improvement in the levels of liver enzymes, a suppression of IL-6 production, as well as histopathological alterations. Therefore, these results suggested that histone preconditioning is able to protect against OJ-induced liver injury in rats.

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Section: Resultssupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Histone preconditioning protects against obstructive jaundice-induced liver injury in rats

Zhou¹,

Ni²,

Liu³

et al. 2014

Experimental and Therapeutic Medicine

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“…Previous studies have demonstrated that corticosteroids can reduce extracellular release of HMGB1 by monocytes in vitro and they can also reduce HMGB1 expression and circulating levels in vivo [23], [24]. However, these findings were not confirmed in patients with rheumatoid arthritis [25].…”

Section: Discussionmentioning

confidence: 89%

Impact of Serum High Mobility Group Box 1 and Soluble Receptor for Advanced Glycation End-Products on Subclinical Atherosclerosis in Patients with Granulomatosis with Polyangiitis

et al. 2014

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The objective of this study was to evaluate whether levels of high mobility group box 1 (HMGB1) in granulomatosis with polyangiitis (GPA) patients are associated with carotid atherosclerosis, related to levels of soluble receptor for advanced glycation end-products (sRAGE) and influenced by immunosuppressive or lipid-lowering therapy. Twenty-three GPA patients and 20 controls were evaluated for HMGB1- and sRAGE levels and for carotid atherosclerosis using ultrasound to determine intima-media thickness (IMT). In vitro the effect of atorvastatin on the production of HMGB1 by lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVEC) was assessed. Serum HMGB1 and sRAGE levels did not differ between patients and controls. A negative correlation was found between sRAGE and maximum IMT but HMGB1 and carotid IMT were not related. HMGB1 levels were reduced in GPA patients on statins and prednisolone. In vitro, atorvastatin reduced HMGB1 levels in supernatants of activated HUVEC. In conclusion, carotid IMT is inversely correlated with sRAGE levels but not with HMGB1 levels. Statins and prednisolone are associated with reduced serum HMGB1 levels and atorvastatin decreases HMGB1 release by activated HUVEC in vitro, indicating an additional anti-inflammatory effect of statins.

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“…Originally, defensin β1 (DB1, encoded by Defb1) is found to be expressed in the lung and urogenital epithelials cells [40][41][42] . Later, DB1 is also found in the liver, especially in the biliary epithelial cells under obstructive jaundice [40,43,44] . DB1 released in circulation may result in ACH.…”

Section: The Elusive Liver Factormentioning

confidence: 99%

Elusive liver factor that causes pancreatic α cell hyperplasia: A review of literature

Zheng

Lucas

et al. 2015

WJGP

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Tumors and cancers of the gastrointestinal tract and pancreas are commonly derived from precursor lesions so that understanding the physiological, cellular, and molecular mechanisms underlying the pathogenesis of precursor lesions is critical for the prevention and treatment of those neoplasms. Pancreatic neuroendocrine tumors (PNETs) can also be derived from precursor lesions. Pancreatic α cell hyperplasia (ACH), a specific and overwhelming increase in the number of α cells, is a precursor lesion leading to PNET pathogenesis. One of the 3 subtypes of ACH, reactive ACH is caused by glucagon signaling disruption and invariably evolves into PNETs. In this article, the existing work on the mechanisms underlying reactive ACH pathogenesis is reviewed. It is clear that the liver secretes a humoral factor regulating α cell numbers but the identity of the liver factor remains elusive. Potential approaches to identify the liver factor are discussed. lesions. One of the precursor lesions, reactive pancreatic α cell hyperplasia is caused by glucagon signaling disruption and invariably evolves into pancreatic neuroendocrine tumors. In this article, the existing work on the mechanisms underlying the novel precursor lesion is reviewed. It is clear that the liver secretes a humoral factor regulating pancreatic α cell numbers but the identity of the liver factor remains elusive. Potential approaches to identify the liver factor are discussed.Yu R, Zheng Y, Lucas MB, Tong YG. Elusive liver factor that causes pancreatic α cell hyperplasia: A review of literature. World J Gastrointest Pathophysiol 2015; 6(4): 131-139 Available from:

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Glucocorticoid Modulates High-Mobility Group Box 1 Expression and Toll-Like Receptor Activation in Obstructive Jaundice

Cited by 18 publications

References 43 publications

Histone preconditioning protects against obstructive jaundice-induced liver injury in rats

Histone preconditioning protects against obstructive jaundice-induced liver injury in rats

Impact of Serum High Mobility Group Box 1 and Soluble Receptor for Advanced Glycation End-Products on Subclinical Atherosclerosis in Patients with Granulomatosis with Polyangiitis

Elusive liver factor that causes pancreatic α cell hyperplasia: A review of literature

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