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  • RESEARCH 4 BUSINESS 2016, Ljubljana, 5 and 6 of May 2016

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    Immunization alone or exposure to diclofenac alone did reviews on viagra pills not cause hepatocyte injury. Prior incubation of diclofenac-exposed hepatocytes with an anti-MHC I antibody afforded partial protection against T-cell-mediated cell killing. Mechanisms of NSAID Hepatotoxicity 353 further purified to a T-cell-enriched fraction. These splenocytes were then combined with isolated and precultured syngeneic hepatocytes and kept in coculture for several days. Prior to being combined with splenocytes, the hepatocytes were exposed to high but nontoxic concentrations (130 µM) of diclofenac, which was biotransformed to reviews on viagra pills a reactive metabolite and subsequently formed covalent adducts to hepatocellular proteins.

    Upon contact with these diclofenac-modified hepatocytes, the primed lymphocytes responded with a proliferative burst and an upregulation of interleukin-2 receptor expression, both specific markers of T-cell activation. Furthermore, the activated T cells were able to kill the diclofenacpretreated hepatocytes as demonstrated by a delayed increase in ALT release from injured hepatocytes. Splenocytes from KLH-diclofenac immunized mice were harvested and either used as a crude splenocyte fraction or Figure 10 Cytotoxic T cells from diclofenac-immunized mice kill hepatocytes previously exposed to diclofenac in vitro, to explore the role of a T-cell-mediated response directed against diclofenac-modified peptides.

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    58:1612–1607. 28:319–381. Isr J Med Sci 1992.

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    ANIMAL MODELS OF DRUG ADDICTION self-administration by rats under extended-access conditions are dose-dependent.