Miquelianin demonstrates antioxidant properties in human plasma, significantly reducing the consumption of lycopene, β-carotene, and α-tocopherol at 50 μM [1]. Miquelianin can penetrate the central nervous system from the small intestine [2]. Miquelianin significantly lowers the production of β-amyloid (Aβ) peptides in primary neuron cultures from the Tg2576 AD mouse model and disrupts the initial protein-protein interactions necessary for forming neurotoxic Aβ oligomers [3]. 0.1 μM miquelianin reduces ROS generation, cAMP and RAS activation, ERK1/2 phosphorylation, and expression of HMOX1, MMP2, and MMP9 genes. It inhibits invasion and MMP-9 induction in MDA-MB-231 breast cancer cells, as well as the binding of [3H]-NA to b2-AR, potentially acting as a dietary chemopreventive agent for stress-related breast cancer by modulating b2-adrenergic signaling [4].
体内研究
Miquelianin treatment significantly enhances basal synaptic transmission and long-term potentiation in the hippocampal formation, improving AD-type deficits compared to vehicle control [3].
体外研究
Miquelianin demonstrates antioxidant properties in human plasma, significantly reducing the consumption of lycopene, β-carotene, and α-tocopherol at 50 μM [1].
Miquelianin can penetrate the central nervous system from the small intestine [2].
Miquelianin significantly lowers the production of β-amyloid (Aβ) peptides in primary neuron cultures from the Tg2576 AD mouse model and disrupts the initial protein-protein interactions necessary for forming neurotoxic Aβ oligomers [3].
0.1 μM miquelianin reduces ROS generation, cAMP and RAS activation, ERK1/2 phosphorylation, and expression of HMOX1, MMP2, and MMP9 genes. It inhibits invasion and MMP-9 induction in MDA-MB-231 breast cancer cells, as well as the binding of [3H]-NA to b2-AR, potentially acting as a dietary chemopreventive agent for stress-related breast cancer by modulating b2-adrenergic signaling [4].
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