Linking Neurodegeneration and the Gut-Brain-Axis: Rutin and Apigenin Attenuate Cytotoxic and Inflammatory Effects of Gut Dysbiosis in Colon Fibroblast Tissue Model
Ashley Dong
Northern Secondary School, Toronto, Canada
Publication date: November 4, 2024
Northern Secondary School, Toronto, Canada
Publication date: November 4, 2024
DOI: http://doi.org/10.34614/JIYRC202419
ABSTRACT
Disruptions to the gut-brain-axis (GBA) are significantly linked to the pathogenesis of neurodegenerative diseases (ND). This study investigated the efficacy of plant flavonoids rutin and apigenin in modulating gut dysbiosis in colon fibroblast tissues, as potential ND-preventative agents. Their effects against fibroblast cytotoxicity, inflammation, and regulation of key proteins involved in neurogenesis were assessed. Most notably, rutin and apigenin increased cell survival against amyloid-beta (AB) toxicity by 26.52% and 22.71% (p<0.0001), respectively. Rutin and apigenin further inhibited inflammation in AB treated cells by 45.80% and 50.34% (p<0.001). However, they were unable to inhibit lipopolysaccharide-induced (LPS) inflammation. Finally, they increased brain-derived neurotrophic factor (BDNF) expression in AB treated cells by 15.46% and 62.15%, respectively (p<0.01). These findings suggest rutin and apigenin as promising multi-target inflammatory modulators of gut dysbiosis in the GBA.
Disruptions to the gut-brain-axis (GBA) are significantly linked to the pathogenesis of neurodegenerative diseases (ND). This study investigated the efficacy of plant flavonoids rutin and apigenin in modulating gut dysbiosis in colon fibroblast tissues, as potential ND-preventative agents. Their effects against fibroblast cytotoxicity, inflammation, and regulation of key proteins involved in neurogenesis were assessed. Most notably, rutin and apigenin increased cell survival against amyloid-beta (AB) toxicity by 26.52% and 22.71% (p<0.0001), respectively. Rutin and apigenin further inhibited inflammation in AB treated cells by 45.80% and 50.34% (p<0.001). However, they were unable to inhibit lipopolysaccharide-induced (LPS) inflammation. Finally, they increased brain-derived neurotrophic factor (BDNF) expression in AB treated cells by 15.46% and 62.15%, respectively (p<0.01). These findings suggest rutin and apigenin as promising multi-target inflammatory modulators of gut dysbiosis in the GBA.
