Trypanosomes

T. congolense, T. b. brucei and T. evansi

Preparation method

The solubility of this compound in DMSO is >30.1 mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 ℃ for several months.

Reacting condition

0.32 ~ 25 μM; 72 hrs

Applications

The IC50 values of Azithromycin for T. congolense, T. b. brucei and T. evansi were 0.19 ± 0.17, 3.69 ± 2.26 and 1.81 ± 1.82 μM, respectively.

Animal models

Mice infected with T. congolense

Dosage form

50, 100, 200, 300 and 400 mg/kg; p.o.

Applications

In mice infected with T. congolense, Azithromycin dose-dependently killed T. congolense, with the initial clearance of the parasites from the peripheral circulation in all treatment groups. However, this was followed by a relapse resulting in the rapid growth of the parasites. On the other hand, the survival rate was significantly prolonged in all treatment groups. A number of mice survived in the 200, 300 and 400 mg/kg Azithromycin groups, while all mice in the control and the 50 and 100 mg/kg Azithromycin groups died.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

Azithromycin is a macrolide antibiotic useful for the treatment of a number of bacterial infections.

Azithromycin (2 μM) augments rhinovirus-induced IFNβ expression in primary bronchial epithelial cells from asthmatics, which is associated with over-expression of RIG-I like receptors and repression of viral replication. Knockdown of MDA5, but not knockdown of RIG-I, diminishes azithromycin (2 μM)-enhanced viral-induced IFNβ expression in asthmatic primary bronchial epithelial cells[1]. Azithromycin specifically reduces MMP-9 mRNA and protein levels without affecting NF-κB in endotoxin-challenged monocytic THP-1 cells[2].

Azithromycin (50 mg/kg) has no effect on bronchoalveolar lavage inflammatory parameters and LDH levels in a mouse model of asthma exacerbation. Azithromycin induces neither general inflammatory parameters nor LDH release in a mouse model of asthma exacerbation, and augments expression of interferon-stimulated genes and the pattern recognition receptor MDA5 but not RIG-I in exacerbating mice[1].

References:
[1]. Menzel M, et al. Azithromycin augments rhinovirus-induced IFNβ via cytosolic MDA5 in experimental models of asthma exacerbation. Oncotarget. 2017 Mar 18.
[2]. Vandooren J, et al. Differential inhibition of activity, activation and gene expression of MMP-9 in THP-1 cells by azithromycin and minocycline versus bortezomib: A comparative study. PLoS One. 2017 Apr 3;12(4):e0174853.