Abstract
We have previously shown that particular phenolic antidiarrheic ingredients, including 2-methoxy-4-methylphenol (2M4MP) and 2-methoxy-4-ethyphenol (2M4EP), but not 2-methoxyphenol (2MP), significantly inhibit cellular maturation and differentiation of the bone-resorbing osteoclasts with concomitant protection of the bone-forming osteoblasts against oxidative stress by hydrogen peroxide (H 2O 2). In the present study, we evaluated the pharmacological actions of these three major phenolic antidiarrheic ingredients on the cellular viability in cultured astrocytes and neurons of the rat brain in vitro. Both 2M4MP and 2M4EP induced more efficient prevention of cell death induced by the brief exposure to 0.1 mM H 2O 2 for 2 h than 2MP upon simultaneous exposure in cultured rat cortical astrocytes. Similarly, both 2M4MP and 2M4EP were more effective than 2MP in significantly protecting the cytotoxicity by brief exposure to 0.1 mM H 2O 2 for 6 h in cultured rat hippocampal neurons, with concomitant suppression of the generation of intracellular reactive oxygen species in neurons exposed to H 2O 2. Moreover, the three ingredients not only significantly prevented cell death in hippocampal neurons exposed to 0.1 mM glutamate for 1 h when determined 48 h after the brief exposure, but also inhibited the generation of intracellular reactive oxygen species and the elevation of intracellular Ca 2+ ions in neurons exposed to glutamate. These results suggest that particular phenolic antidiarrheic ingredients may prevent cell death through a mechanism related to diminution of the neurotoxicity of glutamate in neurons, in addition to eliciting cytoprotection against oxidative stress in astrocytes and neurons, in the rat brain.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.