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71.
Bile acid inhibition of interferon activity in human lymphocytes: no evidence of oxidative stress 总被引:1,自引:0,他引:1
P. PODEVIN M.-C. BLANC M. VAUBOURDOLLE C. VEYRUNES M.-T. BONNEFIS & R. POUPON 《European journal of clinical investigation》1997,27(6):491-496
Cholestasis and bile acids are two factors involved in resistance to interferon therapy in patients with chronic hepatitis C. As bile acids inhibit the biological activity of this cytokine in vitro and are capable of generating oxidative stress in hepatocytes, we investigated the potential involvement of such a mechanism in human lymphocytes. Thus, we evaluated (a) the effects of bile acids (0–200 μmol L−1 ) on lymphocyte reduced glutathione content and malondialdehyde production and (b) the ability of antioxidants to prevent the inhibitory effect of chenodeoxycholic acid on interferon-induced lymphocyte 2',5'-oligoadenylate synthetase activity, an index of the biological activity of interferon. We found that treatment of lymphocytes with bile acids for 24 h did not induce malondialdehyde release or significantly modify cellular reduced glutathione content. Synthetic precursors of glutathione ( N -acetylcysteine and S -adenosylmethionine) and antioxidants (superoxide dismutase and catalase) had no preventive influence on the inhibitory effect of chenodeoxycholic acid on interferon-induced 2',5'-oligoadenylate synthetase activity. These negative results do not provide evidence for the use of glutathione precursors in cholestatic conditions associated with viral diseases. 相似文献
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Two patients with delayed pressure urticaria were studied to define some of the physical and pharmaceutical parameters related to the lesions. Skin tests were performed with a pressure testing; device. Graded pressures were applied from 175 g/cm2 upward for several periods of time to the forearm and back. Induced lesions were clinically identical to spontaneous lesions. The threshold response was related to the amount of pressure, the duration of application and the body site tested. Induced lesions were followed by a refractory period of at least 2 h and up to 48 h. During this period, repeated challenges to an area that reacted previously did not produce any lesion, and, on the contrary, prolonged the refractory period. Any type of intradermal injection (NaCl, lidocaine, compound 48/80, histamine) induced a delayed reaction. But induced delayed lesions were inhibited by intradermal injection of adrenaline before, or after, the pressure stimulus. It is suggested that some intracutaneous targets react to external or intradermal pressure and release chemotactic factors, the effects of which are prevented by vasoconstriction. 相似文献
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