Premium
Capacity of AE to Modulate Nitric Oxide Production Depended on Intercellular Contact
Author(s) -
Mijatovic S.,
MaksimovicIvanic D.,
Miljkovic D. J.,
Harhaji L. J.,
Trajkovic V.
Publication year - 2004
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.0300-9475.2004.01423bj.x
Subject(s) - nitric oxide , macrophage , intracellular , in vitro , apoptosis , chemistry , microbiology and biotechnology , long term potentiation , cell culture , aloe emodin , biophysics , biology , biochemistry , emodin , receptor , genetics , organic chemistry
Aloe emodin (AE) is a naturally occurring compound with wide spectrum of biological properties, including antimicrobial, vasorelaxant, immunosuppressive and anticancer actions. This anthraquinone induces apoptosis in several tumour cell lines with special affinity to tumours of neuroectodermal origin. High amounts of nitric oxide (NO) released by activated macrophages induce tumour cell death. Therefore, we explored the capacity of AE to modulate NO‐mediated antitumour response in vitro . Interestingly, while AE markedly suppressed NO release from macrophages alone, it significantly potentiated NO production in cocultures of macrophages and C6 cells, after 48 h of cultivation. Accordingly, the viability of C6 cells cocultivated with macrophages was reduced in the presence of AE. Moreover, the observed AE‐imposed potentiation of NO production in macrophages was closely related to macrophage culture cell density. According to these data, we proposed that NO modulator capacity of AE strongly depended on intercellular contact, indicating that macrophage antitumour response was not compromised but even potentiated by AE.