Glucocorticoid pretreatment suppresses chemokine expression and inflammatory cell infiltration in cholestatic rats receiving biliary intervention

Hsieh, Chih-Sung; Wang, Pei‐Wen; Lee, Shin-Ye; Huang, Chao‐Cheng; Chang, Nyuk-Kong; Chen, Ching-Mei; Wu, Chia‐Ling; Wang, Hsiu-Chuan; Chuang, Jiin‐Haur

doi:10.1016/j.jpedsurg.2006.05.039

Cited by 11 publications

(11 citation statements)

References 31 publications

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“…Muratore et al have provided the explanation that dexamethasone can alter the hepatic inflammatory cellular profile without changes in matrix degradation during liver repair following biliary decompression [39]. Previous studies by the authors have demonstrated that glucocorticoid treatment suppresses LPSinduced chemokine expression and inflammatory cells infiltration as well as oxidative stress in cholestatic rats receiving biliary intervention [13][14][15]. In this study, we confirm that glucocorticoid treatment results in down-regulation of hepatic HMGB1 expression and release into serum as well as hepatic TLR4 expressions in cholestatic rats.…”

Section: Discussionmentioning

confidence: 99%

“…In our previous studies, we have demonstrated that glucocorticoid administration 2 wk after obstructive jaundice but 10 min prior to administration of LPS or normal saline may alleviate liver injury in cholestatic rats receiving biliary intervention [13][14][15]. However, it is unknown whether glucocorticoid can modulate the upstream HMGB1 and TLR expression in cholestatic liver injury.…”

Section: Introductionmentioning

confidence: 99%

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

Huang

Wang

Tiao

et al. 2011

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Huang

Wang

Tiao

et al. 2011

Journal of Surgical Research

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“…The results of our study highlight the complex network of cytokines that contribute to the initiation and maintenance of inflammation. The anti-inflammatory pattern of leukocyte inhibition presented by rosiglitazone was similar in several aspects to other drugs, including pioglitazone, methotrexate, calcineurin inhibitors (cyclosporine A and tacrolimus), and corticosteroids [23][24][25][26][27]. A common finding in these experimental protocols is that a higher pretreatment dose of rosiglitazone was necessary to inhibit the late influx (48 h) of mononuclear cells in comparison to the dose used to inhibit the early phase (4 h) migration of neutrophils.…”

Section: Discussionmentioning

confidence: 99%

PPAR-Gamma Agonist Rosiglitazone Attenuates the Inflammation Caused by Carrageenan in the Mouse Model of Pleurisy

2011

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The aim of this study was to investigate the anti-inflammatory efficacy of rosiglitazone (ROSI) in a pleurisy model of carrageenan-induced inflammation. Efficacy was monitored in the mouse pleural cavity by evaluating leukocyte migration, exudate concentration, and myeloperoxidase (MPO) and adenosine deaminase (ADA) activities concomitantly with nitrate/nitrite (NOx), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-17A (IL-17A), and vascular endothelial growth factor-alpha (VEGF-α) levels 4 and 48 h after pleurisy induction. In both phases (4 and 48 h) of pleurisy, ROSI inhibited all the inflammation parameters that were tested (p<0.05). These results provide evidence that ROSI was efficacious in inhibiting pro-inflammatory mediators. These anti-inflammatory effects are assumed to mainly result from the inhibition of products released from activated leukocytes, such as MPO, ADA, NOx, TNF-α, IL-1β, IL-17A, and VEGF-α.

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“…The animals were divided randomly into three groups 7 days after the common bile duct ligation (BDL): control group, eight BDL rats submitted to laparotomy without hepatic pedicle occlusion; IR group, eight BDL rats submitted to laparotomy with their left hepatic pedicles exposed while clamped for 30 min (ischemia), followed by 24 h of reperfusion; and DEX group, eight BDL rats received dexamethasone (DEX) intravenously 2 h before induction of hepatic ischemia at a dose of 5 mg/kg body weight [4], followed by hepatic ischemia/reperfusion similar to what was done to the IR group.…”

Section: Animals and Experimental Designmentioning

confidence: 99%

“…Infectious complications, organ dysfunction, and postoperative recovery are improved by administering preoperative steroids in patients undergoing hepatic resection [28]. Glucocorticoid pretreatment suppresses chemokine expression and inflammatory cell infiltration, which consequently alleviate liver injury [4]. DEX is a potent synthetic member of the glucocorticoid drugs.…”

Section: ]mentioning

confidence: 99%

Dexamethasone Pretreatment Attenuates Lung and Kidney Injury in Cholestatic Rats Induced by Hepatic Ischemia/Reperfusion

2011

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Hepatic ischemia followed by reperfusion (IR) results in mild to severe organ injury, in which tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) seem to be involved. Thus, we aim to assess the influence of hepatic ischemia/reperfusion injury on remote organs in addition to cholestasis and consider the possible efficacy of steroid pretreatment in reducing the injury. A common bile duct ligation model was done on 24 male Sprague-Dawley rats. After 7 days, the rats were divided randomly into control group, IR group, and dexamethasone (DEX) group. The IR group showed significant increases in serum alanine aminotransferase, aspartate aminotransferase, and creatinine levels compared with the control and DEX groups. By ELISA techniques, higher levels of TNF-α and IL-1β in lung and kidney tissues were measured in the IR group than in the control and DEX groups, these were verified by immunohistochemistry. The lung histology of the IR group rats showed neutrophil infiltration, interstitial edema, and alveolar wall thickening. Kidney histology of the IR group rats showed vacuolization of the proximal tubular epithelial cells and tubular dilatation with granular eosinophilic casts. Better morphological aspects were observed in the DEX-pretreated animals. Minimal lesions were observed in the control. The results suggest that hepatic ischemia/reperfusion injury in cholestatic rats induced lung and kidney injuries. Pretreatment with dexamethasone reduced the IR-induced injury in addition to cholestasis.

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Glucocorticoid pretreatment suppresses chemokine expression and inflammatory cell infiltration in cholestatic rats receiving biliary intervention

Cited by 11 publications

References 31 publications

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

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

PPAR-Gamma Agonist Rosiglitazone Attenuates the Inflammation Caused by Carrageenan in the Mouse Model of Pleurisy

Dexamethasone Pretreatment Attenuates Lung and Kidney Injury in Cholestatic Rats Induced by Hepatic Ischemia/Reperfusion

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