Active Ingredient: Azithromycin
However, the underlying mechanisms are not been fully elucidated. Tumor necrosis factor-related apoptosis-inducing ligand TRAIL selectively targets tumor cells without damaging healthy cells.
In the present study, we examined whether azithromycin is synergistic with TRAIL, and if so, the underlying mechanisms in colon cancers.
A sulforhoddamine B assay was used to examine cell survival. Western blot analysis was used to detect protein expression levels.
Combination of azithromycin and TRAIL inhibited tumor growth in a manner that could not be explained by additive effects.
Background Azithromycin is a macrolide antibiotic widely used to treat bacterial infection.
Azithromycin accumulates and undergoes slow release in cells, especially in phagocytes, and thus has higher local concentration and longer half-life than older macrolides i.
Recent studies have indicated that azithromycin could produce potent anti-proliferation effect by inducing apoptosis in HeLa cells and SGC-7901 cancer cells.
In addition, it has been reported that antibiotics could affect tumor growth by targeting mitochondria and eradicating cancer stem cells.
Macrolide antibiotics e.
Preclinical and clinical data suggest that clarithromycin in combination with conventional chemotherapeutic agents could produce robust antitumor activities. A range of dosages for each antimicrobial was given to the infected animals on days 2 through 7 5 days of the 21-day survival model.
All untreated control animals survived less than 10 days from infection. Treatment with azithromycin daily dose: 6. We conclude that all agents tested have demonstrated in vivo efficacy in treating acute leptospirosis.
These results provide support for further evaluation of macrolide and ketolide antimicrobial agents in human trials. Leptospirosis is an acute febrile illness caused by spirochetes of the genus Leptospira whose clinical manifestations can range from asymptomatic infection to death.
Afterwards, parasites were placed in 96-well tissue culture plates containing previously collected villous explants.
Toxicity assay Culture supernatants were collected and measurement of lactate dehydrogenase LDH was immediately performed in order to determine cytotoxicity of tested drugs to infected human villous explants.
Measurement of LDH released from the cytosol of lysed cell membranes into the supernatant was performed using a commercial diagnostic kit according to manufacturer instructions LDH Liquiform, LabtestDiagnostica S.
The negative control uninfected control was determined by spontaneous LDH released from uninfected villous explants. Maximum LDH released, defined as positive control total cell lysis, was determined by adding 0.
In parallel, cytokine and hormone levels were measured in supernatants. All subsequent experiments were performed using these drug concentrations.
Hereafter, PSA concentrations will be denoted based on the concentration of pyrimethamine. For antigen retrieval, sections were covered with trypsin solution 0. Cytokine concentration was determined by extrapolation from a standard curve obtained from known concentrations of the respective recombinant cytokines.