Neuroprotective effects of Gnetin H from Paeonia lactiflora via CREB-BDNF pathwa...

연구 요약

Neuroprotective effects of Gnetin H from Paeonia lactiflora via CREB-BDNF pathway restoration in a scopolamine-induced memory deficit model.

European journal of pharmacology 학술지에 발표된 이 연구는 Kim JH, Kim SS, Lee EH 외 연구팀이 수행하였습니다.

이 연구는 'Neuroprotective effects of Gnetin H from Paeonia lactiflora via CREB-BDNF pathway restoration in a scopolamine-induced memory deficit model.'에 대한 과학적 분석을 제공합니다.

핵심 내용

Dementia, a leading cause of disability affecting older adults worldwide, is characterized by memory and cognitive decline associated with dysregulated cholinergic activity and CREB-BDNF signaling. Polyphenols have been investigated for their potential to ameliorate these deficits. Gnetin H, a resveratrol derivative from Paeonia lactiflora seeds with known bioactive properties, has not been evaluated for neuroprotection. Here, we evaluated the neuroprotective actions of Gnetin H in a scopolamine-induced memory deficit model at cellular, slice, and animal levels. In SH-SY5Y neuroblastoma cells, Gnetin H (1 or 15 μM) promoted cell survival under scopolamine treatment. In hippocampal slices, acute bath application of Gnetin H (1.7 μM) enhanced long-term potentiation (LTP) despite scopolamine challenge, indicating preserved synaptic plasticity. In mice, central administration of Gnetin H (10 or 50 ng) restored memory performance in Y-maze, novel object recognition test, and Morris water maze, accompanied by recovery of cholinergic activity and CREB-BDNF signaling. Restoration of CREB-BDNF signaling was abolished by co-treatment of TrkB antagonist ANA-12 in SH-SY5Y cells, which confirmed involvement of TrkB-dependent CREB-BDNF signaling. Finally, Gnetin H rescued scopolamine-induced reductions in DCX-positive neurogenic cells and attenuated astrocytic (GFAP) and microglial (Iba1) reactivity in the hippocampus. In conclusion, Gnetin H exerts neuroprotective effects across cellular, slice, and animal models by enhancing synaptic plasticity (LTP) and restoring CREB-BDNF signaling through TrkB cascade, thereby supporting hippocampal neurogenesis and attenuating scopolamine-induced glial reactivity, with minimal effects under basal conditions.

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