Abstract:
:In the present study, the neuroprotection of osthole (OST) was confirmed. In L-glutamic acid (L-Glu)-damaged HT22 cells, a 3-h pre-incubation with OST-enhanced cell viability suppressed the apoptosis rate; inhibited the activities of caspase-3, caspase-8, and caspase-9; reduced the over-accumulation of intracellular reactive oxygen species; restored the dissipated mitochondrial membrane potential; and regulated the expression levels of B cell lymphoma-2 (Bcl-2), Bax, cleaved poly (ADP-ribose) polymerase (PARP), NF-E2p45-related factor 2 (Nrf2), and its downstream proteins. In amyloid precursor protein/presenilin 1 (APP/PS1) transgenic mice, an 8-week OST administration improved the pathological behaviors related to memory and cognition, and reduced the expression levels of 4-hydroxynonenal, the deposition of β-amyloid peptides and neuronal fiber tangles formed by the high phosphor-Tau in the brain. OST enhanced the expression levels of Nrf2 and its downstream proteins including superoxide dismutase-1 (SOD-1) and heme oxygenase-1 (HO-1). The present data confirmed the protection of OST against AD-like symptoms via modulating oxidative stress, especially Nrf2 signaling.
journal_name
Appl Biochem Biotechnoljournal_title
Applied biochemistry and biotechnologyauthors
Chu Q,Zhu Y,Cao T,Zhang Y,Chang Z,Liu Y,Lu J,Zhang Ydoi
10.1007/s12010-019-03101-2subject
Has Abstractpub_date
2020-02-01 00:00:00pages
634-644issue
2eissn
0273-2289issn
1559-0291pii
10.1007/s12010-019-03101-2journal_volume
190pub_type
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