Protective effects of IL-4 on Bacillus Calmette-Guerin and lipopolysaccharide induced immunological liver injury in mice

Zhang, Nan N.; Huang, Nong Y.; Zhou, Xi Kathy; Luo, Xiao; Liu, Chang Y.; Zhang, Yan; Qiu, Ji; Zhang, Yin B.; Teng, Xiu; Luo, Can; Chen, Xian C.; Kan, Bing; Mao, Yong Qiu; Tong, Ai Ping; Wei, Yu Quan; Li, Jiong

doi:10.1007/s00011-011-0383-9

Cited by 12 publications

(9 citation statements)

References 44 publications

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“…Mouse is not naturally infected with human hepatitis B virus, the relationship between duck hepatitis and human hepatitis were too far. To study the mechanism of immune injury in viral hepatitis by BCG, the preparation of the immune liver injury model is a common method (Zhang et al, 2012). BCG infection has been proven to be a kind of cell-mediated immune response.…”

Section: Discussionmentioning

confidence: 99%

“…Inhibiting NF-jB activation could decrease the induction of NO and decrease the down-regulation of CYP2E1 (Zordoky et al, 2009). Inhibition of NF-jB activation could protect immunological liver from injury (Zhang et al, 2012). Its regulation of transcription of downstream inflammatory cytokine reduced due to the inhibition of NF-jB activation (Lee et al, 2013), thus relieving the inflammation of the liver; in contrast, inhibition of NF-jB could alleviate CYP2E1 down-regulation and reverse the metabolic disorders.…”

Section: Discussionmentioning

confidence: 99%

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Effect of ammonium pyrrolidine dithiocarbamate (PDTC) on NF-κB activation and CYP2E1 content of rats with immunological liver injury

Qin

Cao

et al. 2014

Pharmaceutical Biology

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effect of ammonium pyrrolidine dithiocarbamate (PDTC) on NF-κB activation and CYP2E1 content of rats with immunological liver injury

Qin

Cao

et al. 2014

Pharmaceutical Biology

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“…Many models of drug-induced liver injury mimic the development of various types of hepatitis, including those established with bacillus Chalmette—Guerin (BCG)/lipopolysaccharide (LPS), d -galactosamine ( d -GalN)/LPS, or CCl 4 . The mechanism by which they induce liver injury partly depend on the activation of T cells and macrophages to produce inflammatory cytokines, such as TNF-α, IL-6, IL-1β, and IFN-γ [ 5 , 6 ]. Among these models, ConA-induced liver injury is popular because it is dose dependent and simple to establish.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Astaxanthin on ConA-Induced Autoimmune Hepatitis by the JNK/p-JNK Pathway-Mediated Inhibition of Autophagy and Apoptosis

Xia

Liu

et al. 2015

PLoS ONE

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ObjectiveAstaxanthin, a potent antioxidant, exhibits a wide range of biological activities, including antioxidant, atherosclerosis and antitumor activities. However, its effect on concanavalin A (ConA)-induced autoimmune hepatitis remains unclear. The aim of this study was to investigate the protective effects of astaxanthin on ConA-induced hepatitis in mice, and to elucidate the mechanisms of regulation.Materials and MethodsAutoimmune hepatitis was induced in in Balb/C mice using ConA (25 mg/kg), and astaxanthin was orally administered daily at two doses (20 mg/kg and 40 mg/kg) for 14 days before ConA injection. Levels of serum liver enzymes and the histopathology of inflammatory cytokines and other maker proteins were determined at three time points (2, 8 and 24 h). Primary hepatocytes were pretreated with astaxanthin (80 μM) in vitro 24 h before stimulation with TNF-α (10 ng/ml). The apoptosis rate and related protein expression were determined 24 h after the administration of TNF-α.ResultsAstaxanthin attenuated serum liver enzymes and pathological damage by reducing the release of inflammatory factors. It performed anti-apoptotic effects via the descending phosphorylation of Bcl-2 through the down-regulation of the JNK/p-JNK pathway.ConclusionThis research firstly expounded that astaxanthin reduced immune liver injury in ConA-induced autoimmune hepatitis. The mode of action appears to be downregulation of JNK/p-JNK-mediated apoptosis and autophagy.

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“…NKT cell-initiated injury has been reported to be dependent on the production of IFN-γ [21]. In contrast, the anti-inflammatory IL-4 has been reported to have protective effects on liver injury [22]. In addition, the CD3 + CD49b − IFN-γ + subset, which was produced by T cells, was significantly higher at day 1 than the control (Fig.…”

Section: Tp Treatment Induces Nkt Cell Activationmentioning

confidence: 89%

Activation of natural killer T cells contributes to triptolide-induced liver injury in mice

et al. 2018

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Triptolide (TP) is the main active ingredient of Tripterygium wilfordii Hook.f, which has attracted great interest due to its promising efficacy for autoimmune diseases and tumors. However, severe adverse reactions, especially hepatotoxicity, have restricted its approval in the market. In the present study we explored the role of hepatic natural killer T (NKT) cells in the pathogenesis of TP-induced liver injury in mice. TP (600 μg/kg/day, i.g.) was administered to female mice for 1, 3, or 5 days. We found that administration of TP dose-dependently induced hepatotoxicity, evidenced by the body weight reduction, elevated serum ALT and AST levels, as well as significant histopathological changes in the livers. However, the mice were resistant to the development of TP-induced liver injury when their NKT cells were depleted by injection of anti-NK1.1 mAb (200 μg, i.p.) on days -2 and -1 before TP administration. We further revealed that TP administration activated NKT cells, dominantly releasing Th1 cytokine IFN-γ, recruiting neutrophils and macrophages, and leading to liver damage. After anti-NK1.1 injection, however, the mice mainly secreted Th2 cytokine IL-4 in the livers and exhibited a significantly lower percentage of hepatic infiltrating neutrophils and macrophages upon TP challenge. The activation of NKT cells was associated with the upregulation of Toll-like receptor (TLR) signaling pathway. Collectively, these results demonstrate a novel role of NKT cells contributing to the mechanisms of TP-induced liver injury. More importantly, the regulation of NKT cells may promote effective measures that control drug-induced liver injury.

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Protective effects of IL-4 on Bacillus Calmette-Guerin and lipopolysaccharide induced immunological liver injury in mice

Abstract: IL-4 may protect mice against BCG/LPS-induced immune liver injury, besides ERK and NF-κB signal pathways were involved in the effects.

Cited by 12 publications

References 44 publications

Effect of ammonium pyrrolidine dithiocarbamate (PDTC) on NF-κB activation and CYP2E1 content of rats with immunological liver injury

Effect of ammonium pyrrolidine dithiocarbamate (PDTC) on NF-κB activation and CYP2E1 content of rats with immunological liver injury

Protective Effects of Astaxanthin on ConA-Induced Autoimmune Hepatitis by the JNK/p-JNK Pathway-Mediated Inhibition of Autophagy and Apoptosis

Activation of natural killer T cells contributes to triptolide-induced liver injury in mice

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