Compounds > amphotericin-b--deoxycholate-drug-combination

amphotericin-b--deoxycholate-drug-combination and arabinogalactan

amphotericin-b--deoxycholate-drug-combination has been researched along with arabinogalactan* in 1 studies

Other Studies

1 other study(ies) available for amphotericin-b--deoxycholate-drug-combination and arabinogalactan

Article	Year
Induction of interleukin-1beta, tumour necrosis factor-alpha and apoptosis in mouse organs by amphotericin B is neutralized by conjugation with arabinogalactan. The Journal of antimicrobial chemotherapy, 2005, Volume: 55, Issue:5 To investigate the possibilities that: (i) organ toxicity of amphotericin B-deoxycholate (AMB-DOC) is related to induction of interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and apoptosis in target organs; and (ii) the reduced toxicity resulting from the conjugation of AMB with water-soluble arabinogalactan (AMB-AG), is related to modulation of these parameters.. Organ expression of IL-1beta and TNF-alpha was evaluated by enzyme-linked immunosorbent assay (ELISA) in mouse organ biological fluids and in situ by immunohistochemistry. Tissue damage was evaluated histologically, and apoptosis was demonstrated by terminal dUTP nick end-labelling (TUNEL) staining. AMB-AG conjugate was compared with the micellar (AMB-DOC) and liposomal (AmBisome) AMB formulations.. Treatment with AMB-AG or AmBisome caused no observable histopathological damage in the kidneys. In contrast, treatment with AMB-DOC resulted in disruptive changes and apoptosis in renal tubular cells. These effects were found to correlate with induction of high levels of IL-1beta and TNF-alpha in kidney lysates. Unlike AMB-AG, AMB-DOC also induced enhanced IL-1beta and TNF-alpha expression in lysates of lungs, brain, liver and spleen. The marked elevation of these inflammation-apoptosis-promoting cytokines after treatment with AMB-DOC may mediate its systemic and local renal damage. Treatment with AMB-AG (but not AmBisome) appears to uniquely modulate the in situ expression of IL-1beta and enhance secretion of TNF-alpha in kidneys, effects possibly involved in prevention of apoptosis.. AMB-related toxicity is associated with induction of IL-1beta, TNF-alpha and apoptosis in organs. These effects were not observed with AMB-AG conjugate, suggesting its potential as a safer formulation for therapy. Topics: Amphotericin B; Animals; Antifungal Agents; Apoptosis; Cytokines; Deoxycholic Acid; Drug Combinations; Galactans; Interleukin-1; Kidney; Male; Mice; Mice, Inbred BALB C; Tumor Necrosis Factor-alpha	2005

Article

Year

Induction of interleukin-1beta, tumour necrosis factor-alpha and apoptosis in mouse organs by amphotericin B is neutralized by conjugation with arabinogalactan.

The Journal of antimicrobial chemotherapy, 2005, Volume: 55, Issue:5

To investigate the possibilities that: (i) organ toxicity of amphotericin B-deoxycholate (AMB-DOC) is related to induction of interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and apoptosis in target organs; and (ii) the reduced toxicity resulting from the conjugation of AMB with water-soluble arabinogalactan (AMB-AG), is related to modulation of these parameters.. Organ expression of IL-1beta and TNF-alpha was evaluated by enzyme-linked immunosorbent assay (ELISA) in mouse organ biological fluids and in situ by immunohistochemistry. Tissue damage was evaluated histologically, and apoptosis was demonstrated by terminal dUTP nick end-labelling (TUNEL) staining. AMB-AG conjugate was compared with the micellar (AMB-DOC) and liposomal (AmBisome) AMB formulations.. Treatment with AMB-AG or AmBisome caused no observable histopathological damage in the kidneys. In contrast, treatment with AMB-DOC resulted in disruptive changes and apoptosis in renal tubular cells. These effects were found to correlate with induction of high levels of IL-1beta and TNF-alpha in kidney lysates. Unlike AMB-AG, AMB-DOC also induced enhanced IL-1beta and TNF-alpha expression in lysates of lungs, brain, liver and spleen. The marked elevation of these inflammation-apoptosis-promoting cytokines after treatment with AMB-DOC may mediate its systemic and local renal damage. Treatment with AMB-AG (but not AmBisome) appears to uniquely modulate the in situ expression of IL-1beta and enhance secretion of TNF-alpha in kidneys, effects possibly involved in prevention of apoptosis.. AMB-related toxicity is associated with induction of IL-1beta, TNF-alpha and apoptosis in organs. These effects were not observed with AMB-AG conjugate, suggesting its potential as a safer formulation for therapy.

Topics: Amphotericin B; Animals; Antifungal Agents; Apoptosis; Cytokines; Deoxycholic Acid; Drug Combinations; Galactans; Interleukin-1; Kidney; Male; Mice; Mice, Inbred BALB C; Tumor Necrosis Factor-alpha

2005