Perturbation of liver function markers and serum electrolytes associated with Echinococcus granulosus infection in sheep

Abstract Background & Aims: TGF-β not only inhibits the function of NK cells, but also promotes liver fibrosis. It is unclear whether the inhibition of TGF-β signaling pathway could relieve the CE-related liver fibrosis.Methods: By using the model of CE infected mouse liver, the effect of the infection of CE exerted on NK cells was identified. In vivo, SB525334 and Pirfenidone were applied to intervene the TGF-β signaling pathway.Results: During the infection of Echinococcus granulosus, the inhibitory receptors on the surface of NK cells increased, while the activated receptors decreased. TGF-β1 secretion was increased in liver tissues and mainly derived from macrophages. At the same time, the combination of drugs could also reduce the expression of TGF-β1 signaling pathway-related proteins and collagen. For the secretion of TGF-β1, only the pirfenidone group had an depressing effect. In addition, the combination of drugs can reduce liver cell damage and restore liver function.Conclusions: During the infection the of Echinococcus granulosus, the dysfunction of NK cells may be caused by increased secretion of TGF-β1 from macrophages. Echinococcus granulosus infection was a process of occupying lesions. This persistent pressure was accompanied by senescent hepatocytes. Senescent hepatocytes induced the secretion of TGF-β1 derived from macrophages, and promoted the activation of hepatic stellate cells and accelerated Echinococcus granulosus-associated liver fibrosis. By combining pirfenidone and SB525334, liver function, senescent hepatocytes, fibrosis associated with Echinococcus granulosus infection could be alleviated. Moreover, the functional status of NK cells also received partially amelioration. In summary, our work offered an experimental basis for clinical treatment.

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Acetaminophen: Macula densa hypersecretory activity by induced hepatotoxicity

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010012895x ◽

1987 ◽

Vol 45 ◽

pp. 934-935

Author(s):

S.S. Poolsawat ◽

C.A. Huerta ◽

S.TY. Lae ◽

G.A. Miranda

Keyword(s):

Cell Proliferation ◽

Liver Function ◽

Chronic Inflammation ◽

Foam Cell ◽

Term Effect ◽

Short Term ◽

Drug Induced ◽

Experimental Induction ◽

Tissue Alterations ◽

Toxic Responses

Introduction. Experimental induction of altered histology by chemical toxins is of particular importance if its outcome resembles histopathological phenomena. Hepatotoxic drugs and chemicals are agents that can be converted by the liver into various metabolites which consequently evoke toxic responses. Very often, these drugs are intentionally administered to resolve an illness unrelated to liver function. Because of hepatic detoxification, the resulting metabolites are suggested to be integrated into the macromolecular processes of liver function and cause an array of cellular and tissue alterations, such as increased cytoplasmic lysis, centrilobular and localized necroses, chronic inflammation and “foam cell” proliferation of the hepatic sinusoids (1-4).Most experimentally drug-induced toxicity studies have concentrated primarily on the hepatic response, frequently overlooking other physiological phenomena which are directly related to liver function. Categorically, many studies have been short-term effect investigations which seldom have followed up the complications to other tissues and organs when the liver has failed to function normally.

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