International immunopharmacology
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Int. Immunopharmacol. · Dec 2004
Piperine is a potent inhibitor of nuclear factor-kappaB (NF-kappaB), c-Fos, CREB, ATF-2 and proinflammatory cytokine gene expression in B16F-10 melanoma cells.
Immune regulation, induction of various inflammatory and growth regulatory genes such as IL-1beta, IL-6, TNF-alpha and GM-CSF require activation of transcription factors such as nuclear factor-kappaB (NF-kappaB), activated transcription factor (ATF-2), c-Fos and cAMP response element-binding protein (CREB). Untreated B16F-10 cells produce very high amount of proinflammatory cytokines such as IL-1beta, IL-6, TNF-alpha and GM-CSF. Piperine treatment significantly reduced the above proinflammatory cytokines. ⋯ Piperine at a concentration of 2.5, 5 and 10 microg/ml inhibited the collagen matrix invasion of B16F-10 melanoma cells in a dose-dependent manner. Piperine could inhibit the matrix metalloproteinase production which was demonstrated by zymographic analysis. We found that the nuclear translocation of p65, p50, c-Rel subunits of NF-kappaB and other transcription factors such as ATF-2, c-Fos and CREB were inhibited by the treatment of piperine.
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Int. Immunopharmacol. · Dec 2004
Nicotine could augment adhesion molecule expression in human endothelial cells through macrophages secreting TNF-alpha, IL-1beta.
Nicotine, the major immunomodulatory components of cigarette smoking, is among the leading risk factors in atherosclerosis and various other diseases. The subject of this study is to observe how nicotine affects the function of macrophages and vascular endothelial cells. The changes of nicotine on releasing of cytokines from Ana-1 were detected by radio-immunoassay (RIA) or enzyme-link immunosorbent assay (ELISA). ⋯ Treatment of HUVECs with anti-TNF-alpha, anti-IL-1beta antibodies pre-neutralized supernatant of Ana-1 could block monocytes adhesion. In conclusion, our findings suggest that nicotine could augment macrophages releasing TNF-alpha and IL-1beta, furthermore TNF-alpha and IL-1beta could up-regulate the expression of adhesion molecule and increase adhesion of monocytes to HUVECs. These might be one of the reasons that leaded to endothelial dysfunction.
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Int. Immunopharmacol. · Dec 2004
Comparative StudyEffect of Tinospora cordifolia on the cytokine profile of angiogenesis-induced animals.
The antiangiogenic activity of Tinospora cordifolia was studied using in vivo as well as in vitro models. In vivo antiangiogenic activity was studied using B16F10 melanoma cell-induced capillary formation in animals. Intraperitoneal administration of the extract at a concentration of 20 mg/kg significantly inhibited the tumour directed capillary formation induced by melanoma cells. ⋯ Moreover, using an in vitro rat aortic ring assay, it was observed that the extract at nontoxic concentrations inhibited the production of proangiogenic factors from B16F10 melanoma cells. Direct treatment of the extract also inhibits the microvessel outgrowth from the aortic ring. Hence, the observed antiangiogenic activity of the plant T. cordifolia is related, at least in part, to the regulation of the levels of these cytokines and growth factors in the blood of the angiogenesis-induced animal.