Early induced, high-level interleukin-6 expression in the rat peritoneal cavity into which a hepatotoxicant carbon tetrachloride was administered

Zuinen, Ryoji; Yamaji, Kenzaburo; Aoki, Miho; Chikuma, Toshiyuki; Hara, Hiroshi

doi:10.1016/j.toxlet.2007.02.003

Cited by 7 publications

(2 citation statements)

References 24 publications

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“…After i.p. CCl 4 administration, plasma IL6 level rapidly increased as previously shown [21] but values in WT and Gas6 À/À mice were not significantly different at 24 and 48 h (237 ± 92 versus 271 ± 132 pg/ml, respectively). However, we revealed a significantly reduced IL6 protein in liver of deficient mice (Fig.…”

Section: Gas6 Deficiency Reduces Kupffer Cell Activation and Cytokinesupporting

confidence: 78%

Growth arrest-specific protein 6 deficiency impairs liver tissue repair after acute toxic hepatitis in mice

Lafdil

Chobert

Deveaux

et al. 2009

Journal of Hepatology

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Section: Gas6 Deficiency Reduces Kupffer Cell Activation and Cytokinesupporting

confidence: 78%

Growth arrest-specific protein 6 deficiency impairs liver tissue repair after acute toxic hepatitis in mice

Lafdil

Chobert

Deveaux

et al. 2009

Journal of Hepatology

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“…IL-6 also binds to both membrane-bound IL-6 receptor and soluble IL-6 receptor to trigger NF-κB- and STAT3-dependent hepatic regeneration [36, 37]. TGF-β 1 is mainly a pro-fibrotic factor in chronic liver disease, e.g., fatty liver disease.…”

Section: Discussionmentioning

confidence: 99%

S-allylmercaptocysteine reduces carbon tetrachloride-induced hepatic oxidative stress and necroinflammation via nuclear factor kappa B-dependent pathways in mice

et al. 2011

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PurposeTo study the protective effects and underlying molecular mechanisms of SAMC on carbon tetrachloride (CCl4)-induced acute hepatotoxicity in the mouse model.MethodsMice were intraperitoneally injected with CCl4 (50 μl/kg; single dose) to induce acute hepatotoxicity with or without a 2-h pre-treatment of SAMC intraperitoneal injection (200 mg/kg; single dose). After 8 h, the blood serum and liver samples of mice were collected and subjected to measurements of histological and molecular parameters of hepatotoxicity.ResultsSAMC reduced CCl4-triggered cellular necrosis and inflammation in the liver under histological analysis. Since co-treatment of SAMC and CCl4 enhanced the expressions of antioxidant enzymes, reduced the nitric oxide (NO)-dependent oxidative stress, and inhibited lipid peroxidation induced by CCl4. SAMC played an essential antioxidative role during CCl4-induced hepatotoxicity. Administration of SAMC also ameliorated hepatic inflammation induced by CCl4 via inhibiting the activity of NF-κB subunits p50 and p65, thus reducing the expressions of pro-inflammatory cytokines, mediators, and chemokines, as well as promoting pro-regenerative factors at both transcriptional and translational levels.ConclusionsOur results indicate that SAMC mitigates cellular damage, oxidative stress, and inflammation in CCl4-induced acute hepatotoxicity mouse model through regulation of NF-κB. Garlic or garlic derivatives may therefore be a potential food supplement in the prevention of liver damage.

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Oxidative stress and inflammatory responses in the liver of swamp eel (Monopterus albus) exposed to carbon tetrachloride

et al. 2018

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Early induced, high-level interleukin-6 expression in the rat peritoneal cavity into which a hepatotoxicant carbon tetrachloride was administered

Cited by 7 publications

References 24 publications

Growth arrest-specific protein 6 deficiency impairs liver tissue repair after acute toxic hepatitis in mice

Growth arrest-specific protein 6 deficiency impairs liver tissue repair after acute toxic hepatitis in mice

S-allylmercaptocysteine reduces carbon tetrachloride-induced hepatic oxidative stress and necroinflammation via nuclear factor kappa B-dependent pathways in mice

Oxidative stress and inflammatory responses in the liver of swamp eel (Monopterus albus) exposed to carbon tetrachloride

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