Avarol protects HT22 neuronal cells from BV2 microglia cell-derived neuroinflamm...

연구 요약

Avarol protects HT22 neuronal cells from BV2 microglia cell-derived neuroinflammation in lipopolysaccharide-induction model.

Immunopharmacology and immunotoxicology 학술지에 발표된 이 연구는 Gu JY, Kang JY, Lee WY 외 연구팀이 수행하였습니다.

이 연구는 'Avarol protects HT22 neuronal cells from BV2 microglia cell-derived neuroinflammation in lipopolysaccharide-induction model.'에 대한 과학적 분석을 제공합니다.

핵심 내용

BACKGROUND: Pathological neuroinflammation is a critical factor that disrupts neuronal activity and, when sustained, ultimately contributes to neuronal death. Among the primary mediators of neuroinflammation, microglia play a central role in modulating brain immunity. However, their overactivation is closely associated with neuronal damage and structural remodeling of brain tissue, leading to the onset and progression of various neurodegenerative diseases. MATERIALS AND METHODS: We investigated the neuroprotective effects of avarol, a marine-derived sesquiterpenoid, focusing on its ability to inhibit lipopolysaccharide (LPS)-induced overactivation of BV2 microglial cells and its subsequent impact on neuronal activity in HT-22 hippocampal neuronal cells. RESULTS: Pretreatment with avarol significantly attenuated the LPS-induced release of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), as well as oxidative stress markers such as reactive oxygen species (ROS) and nitric oxide (NO). These inhibitory effects were further substantiated by a dose-dependent reduction in nuclear translocation of nuclear factor-kappa B (NF-κB), a key transcription factor involved in the inflammatory signaling cascade. Regarding the interaction between microglia and neurons, both conditioned medium and co-culture systems demonstrated that avarol significantly attenuated alterations in neuronal plasticity-related molecules-such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF)-induced by activated microglia. CONCLUSIONS: Overall, these findings suggest that avarol exerts neuroprotective effects through the modulation of microglia-mediated neuroinflammation. Importantly, avarol's capacity to traverse the blood-brain barrier highlights its potential as an effective pharmacological agent in mitigating neuroinflammation-associated neurological disorders.

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