ArticleFrontiers in pharmacology2025
Isoliensinine confers neuroprotection and alleviates LPS-induced neuroinflammation in microglia by regulating the MAPK/NF-κB signaling.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Unlocking the Power of Plant-Derived Natural Products: Therapeutic Benefits for Cognitive Health and Neuropsychiatric Symptoms in Dementia-Related Diseases.Plants (Basel, Switzerland) · 2026Review
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7 authors.
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Abstract
Background: The increasing aged population poses issues in the management of age-related disorders, notably Alzheimer's disease (AD), which significantly affects the health and quality of life of seniors. Neuroinflammation is a significant factor in Alzheimer's disease pathogenesis. Isoliensinine (ISO), a bisbenzylisoquinoline alkaloid derived from lotus seed embryos, exhibits antioxidant and anti-inflammatory effects. Nonetheless, its function in neuroinflammation has yet to be investigated. Methods: We examined the impact of ISO on LPS-induced neuroinflammation in BV2 microglial cells by using biological tests. Western blotting confirmed ISO's influence on MAPK/NF-κB signaling pathways. In addition, oxidative stress markers and JC-1 staining were employed to assess the impact of ISO on LPS-induced oxidative stress and mitochondrial dysfunction in BV2 cells. Results: ISO markedly diminished LPS-induced neuroinflammation in BV2 cells through the modulation of the MAPK/NF-κB pathway. Conditioned media derived from ISO-treated BV2 cells enhanced the vitality of HT-22 cells. ISO also alleviated oxidative stress and mitochondrial dysfunction. Conclusion: Our findings indicate that ISO mitigates neuroinflammation by inhibiting MAPK/NF-κB signaling and provides neuroprotection by diminishing oxidative stress and mitochondrial impairment. These effects collectively enhance its neuroprotective capacity, indicating that ISO may represent a potential candidate for further investigation in AD.
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