Several studies provide evidence that reactive oxygen species (ROS) are key mediators of various
neurological disorders. Anthocyanins are polyphenolic compounds and are well known for their antioxidant
and neuroprotective effects. In this study, we investigated the neuroprotective effects of anthocyanins
(extracted from black soybean) against lipopolysaccharide (LPS)-induced ROS-mediated
neuroinflammation and neurodegeneration in the adult mouse cortex. Intraperitoneal injection of LPS
(250 mg/kg) for 7 days triggers elevated ROS and oxidative stress, which induces neuroinflammation and
neurodegeneration in the adult mouse cortex. Treatment with 24 mg/kg/day of anthocyanins for 14 days
in LPS-injected mice (7 days before and 7 days co-treated with LPS) attenuated elevated ROS and
oxidative stress compared to mice that received LPS-injection alone. The immunoblotting results showed
that anthocyanins reduced the level of the oxidative stress kinase phospho-c-Jun N-terminal Kinase 1 (pJNK).
The immunoblotting and morphological results showed that anthocyanins treatment significantly
reduced LPS-induced-ROS-mediated neuroinflammation through inhibition of various inflammatory
mediators, such as IL-1b, TNF-a and the transcription factor NF-kB. Anthocyanins treatment also reduced
activated astrocytes and microglia in the cortex of LPS-injected mice, as indicated by reductions in GFAP
and Iba-1, respectively. Anthocyanins also prevent overexpression of various apoptotic markers, i.e., Bax,
cytosolic cytochrome C, cleaved caspase-3 and PARP-1. Immunohistochemical fluoro-jade B (FJB) and
Nissl staining indicated that anthocyanins prevent LPS-induced neurodegeneration in the mouse cortex.
Our results suggest that dietary flavonoids, such as anthocyanins, have antioxidant and neuroprotective
activities that could be beneficial to various neurological disorders.