Nutrients · 8 authors, 5 centres
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This in vitro study used mouse neural stem cells and microglia to show that Kaempferia parviflora extracts protect against amyloid-beta-induced neuroinflammation and promote neuronal differentiation. However, the findings are limited to cell cultures and require further investigation in animal models and humans.
Alzheimer's disease involves neuroinflammation and impaired neurogenesis, with amyloid-beta (Aβ) peptides contributing to neuronal damage. Kaempferia parviflora (KP) has known anti-inflammatory properties, but its effects on Aβ-induced neurotoxicity and neurogenesis were unexplored. Methods: This in vitro study used mouse neural stem cells (NE-4C) and microglial cells (BV-2) in monoculture and co-culture models. Cells were treated with Aβ42 peptides (0.25–20 µM) and KP extracts (KP1–KP5 fractions, 0.5–8 µg/mL). Assays measured cytotoxicity (XTT, ATP), inflammation (IL-6, nitrite, ROS), and neurogenesis markers (βIII-tubulin, MAP-2 mRNA). Key Results: KP1, KP2, and KP3 fractions (containing DMF, PMF, TMF) significantly reduced Aβ42-induced cytotoxicity, inflammation (IL-6, NO), and oxidative stress in both monoculture and co-culture. They also restored βIII-tubulin and MAP-2 expression, indicating protection against Aβ42-inhibited neuronal differentiation. Limitations: The study is limited to in vitro cell cultures, so results may not directly translate to human clinical outcomes; specific molecular mechanisms and individual compound contributions were not fully elucidated. Implications: KP extracts show neuroprotective and neurogenic potential against Aβ42-mediated damage, warranting further in vivo studies to explore therapeutic applications for Alzheimer's disease.
