Prevention of carbon tetrachloride-induced rat liver injury by soluble tumor necrosis factor receptor

Czaja, Mark J.; Xu, Jun; E, Alt

doi:10.1016/0016-5085(95)90149-3

Cited by 179 publications

(114 citation statements)

References 27 publications

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“…10 These results differ from studies performed in the rat, showing a role for TNF-␣ in the pathogenesis of CCl 4 hepatitis 9 or a role for Kupffer cells, the presumed cellular source of TNF-␣ in this model. 1 Higher doses of CCl 4 used in these studies 9 and the presence of a ''physiological'' endotoxemia in rats, 39 are two factors which may have led to increased TNF-␣ secretion in these rat' s models and may account for this discrepancy. Our results also show that the increased neutrophilic infiltration observed in centrilobular necrotic areas of IL-10 KO mice is mainly a result of an enhanced TNF-␣ production.…”

Section: Discussionmentioning

confidence: 96%

“…Among them, tumor necrosis factor-alpha (TNF-␣) has emerged as a major endogenous mediator of hepatotoxicity in several experimental models of liver injury, [5][6][7] through direct cytotoxicity 8 and the triggering of an inflammatory cascade. Nevertheless, the participation of TNF-␣ in the pathogenesis of CCl 4 liver injury is still debated because neutralization of TNF-␣ protected rats against subsequent CCl 4 hepatotoxicity, 9 although it did not provide such a protective effect in mice. 10 Severe liver damage is followed by a phase of liver repair wherein surrounding hepatocytes proliferate and the extracellular matrix synthesis increases.…”

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confidence: 99%

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Interleukin-10 controls neutrophilic infiltration, hepatocyte proliferation, and liver fibrosis induced by carbon tetrachloride in mice

Louis¹,

Laethem²,

et al. 1998

Hepatology

245

161

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The role of the anti-inflammatory cytokine interleukin-10 (IL-10) was investigated in the mouse model of liver injury induced by carbon tetrachloride (CCl 4 ). To address the role of endogenous IL-10 production, acute hepatitis was induced by CCl 4 in C57Bl/6 IL-10 gene knock out (KO) and wild-type (WT) mice. After CCl 4 challenge, serum and liver levels of tumor necrosis factor-alpha (TNF-␣) and serum levels of transforming growth factor-beta 1 (TGF-␤1) increased and were significantly higher in IL-10 KO mice, whereas IL-6 serum levels were only slightly increased compared with WT mice. At histological examination, the livers disclosed a significantly more prominent neutrophilic infiltration in IL-10 KO mice 12 and 24 hours after CCl 4 injection. In contrast, hepatocyte necrosis, evaluated by histological examination and serum alanine aminotransferase levels, was only marginally affected. The proliferative response of hepatocytes, assessed by the proliferating cell nuclear-antigen labeling index, was significantly increased in IL-10 KO mice, compared with WT mice 48 hours after CCl 4 injection. Finally, repeated CCl 4 injections led to more liver fibrosis in IL-10 KO mice after 7 weeks. In conclusion, endogenous IL-10 marginally affects the hepatocyte necrosis although it controls the acute inflammatory burst induced by CCl 4 . During liver repair, it limits the proliferative response of hepatocytes and the development of fibrosis. (HEPATOLOGY 1998;28:1607-1615.)

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

Interleukin-10 controls neutrophilic infiltration, hepatocyte proliferation, and liver fibrosis induced by carbon tetrachloride in mice

Louis¹,

Laethem²,

et al. 1998

Hepatology

245

161

View full text Add to dashboard Cite

show abstract

“…In the liver, TNF has been implicated as a mediator of hepatocellular dysfunction and death following toxic injury, viral hepatitis, and sepsis (2)(3)(4)(5)(6)(7)(8). It is thought that such pathological conditions lead to the release of TNF by hepatic macrophages, with resultant paracrine actions on other liver cells (9).…”

mentioning

confidence: 99%

Activation of Potassium and Chloride Channels by Tumor Necrosis Factor α

Nietsch

Roe

Fiekers

et al. 2000

Journal of Biological Chemistry

107

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Despite abundant evidence for changes in mitochondrial membrane permeability in tumor necrosis factor (TNF)-mediated cell death, the role of plasma membrane ion channels in this process remains unclear. These studies examine the influence of TNF on ion channel opening and death in a model rat liver cell line (HTC). TNF (25 ng/ml) elicited a 2-and 5-fold increase in K ؉ and Cl ؊ currents, respectively, in HTC cells. These increases occurred within 5-10 min after TNF exposure and were inhibited either by K ؉ or Cl ؊ substitution or by K ؉ channel blockers (Ba 2؉ , quinine, 0.1 mM each) or Cl ؊ channel blockers (10 M 5-nitro-2-(3-phenylpropylamino)benzoic acid and 0.1 mM N-phenylanthranilic acid), respectively. TNF-mediated increases in K ؉ and Cl ؊ currents were each inhibited by intracellular Ca 2؉ chelation (5 mM EGTA), ATP depletion (4 units/ml apyrase), and the protein kinase C (PKC) inhibitors chelerythrine (10 M) or PKC 19 -36 peptide (1 M). In contrast, currents were not attenuated by the calmodulin kinase II 281-309 peptide (10 M), an inhibitor of calmodulin kinase II. In the presence of actinomycin D (1 M), each of the above ion channel blockers significantly delayed the progression to TNF-mediated cell death. Collectively, these data suggest that activation of K ؉ and Cl ؊ channels is an early response to TNF signaling and that channel opening is Ca 2؉ -and PKC-dependent. Our findings further suggest that K ؉ and Cl ؊ channels participate in pathways leading to TNF-mediated cell death and thus represent potential therapeutic targets to attenuate liver injury from TNF.

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“…23) Soluble TNF-a receptor prevented the increase in serum ALT 24 h after CCl 4 intoxication and thereafter, showing an important role of TNF-a in the second phase of liver cell injury. 24) Upregulation of TNF-a associated with the induction of COX-2, 25,26) products of which might have a conceivable link between inflammatory response and oxidative injury. 5) Overexpression of COX-2 in the mouse liver resulted in a marked induction of the proinflammatory cytokines such as TNF-a, IL-1b, and IL-6, inducing hepatitis, which was recovered by celecoxib administration.…”

Section: Discussionmentioning

confidence: 99%

Effect of Celecoxib, a Selective Cyclooxygenase-2 Inhibitor on Carbon Tetrachloride Intoxication in Rats

Washino

Koga

Kitamura

et al. 2010

Biological & Pharmaceutical Bulletin

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CCl 4 (0.5 ml/kg as CCl 4 ) was orally administered to rats. Twelve hours after administration of CCl 4 , plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, indicators of liver necrosis, were significantly higher than those in the control group showing that active liver necrosis took place. At the same time the level of liver vitamin C was decreased significantly compared to that in the control group. Oral administration of 100 mg/kg each of celecoxib 3 and 8 h after CCl 4 treatment did not change plasma ALT and AST and liver vitamin C levels 12 h after CCl 4 treatment, but 24 h after CCl 4 treatment, significantly decreased plasma ALT and AST levels and elevated liver vitamin C level. These finding suggested that celecoxib effectively ameliorated the necrotic action and the oxidative stress induced by CCl 4 in the second phase. Although the plasma levels of all ceramide species were significantly increased 24 h after CCl 4 intoxication, treatment with celecoxib significantly reduced the total ceramide concentration in plasma. These results indicated that celecoxib significantly ameliorated the toxicity of CCl 4 in the second phase.

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Prevention of carbon tetrachloride-induced rat liver injury by soluble tumor necrosis factor receptor

Cited by 179 publications

References 27 publications

Interleukin-10 controls neutrophilic infiltration, hepatocyte proliferation, and liver fibrosis induced by carbon tetrachloride in mice

Interleukin-10 controls neutrophilic infiltration, hepatocyte proliferation, and liver fibrosis induced by carbon tetrachloride in mice

Activation of Potassium and Chloride Channels by Tumor Necrosis Factor α

Effect of Celecoxib, a Selective Cyclooxygenase-2 Inhibitor on Carbon Tetrachloride Intoxication in Rats

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