7,8-Dihydroxyflavone (7,8-DHF) is a potent and selective TrkB agonist that mimics the physiological actions of Brain-derived neurotrophic factor (BDNF). 7,8-DHF (500 nM) protected primary neurons from Aβ-induced toxicity and promoted dendrite branching and synaptogenesis. Chronic oral administration of 7,8-DHF activated TrkB signaling and prevented Aβ deposition in transgenic mice that coexpress five familial Alzheimer's disease mutations (5XFAD mice). Moreover, 7,8-DHF inhibited the loss of hippocampal synapses, restored synapse number and synaptic plasticity, and prevented memory deficits[3]. 7,8-DHF activated the Nrf2 signaling pathway in primary chondrocytes[4]. 7,8-DHF might be capable of alleviating the jejunal contractile damage caused by IR (ischaemia-reperfusion) through activation of TrkB and augmentation of M3 expression[5]. 7,8-DHF (5 mg/kg; i.p.) administration conferred beneficial effects against alcohol and HFD-induced memory deficit via its unique antioxidant, anti-inflammatory, anti-apoptotic potential, along with the activation of TrkB/BDNF signaling pathway in the hippocampus[6].
7,8-Dihydroxyflavone/7,8-二羟基黄酮水合物 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Primary hippocampal neurons
250 nM
Activate TrkB receptor
Transl Neurodegener. 2016 Jan 6;5:2.
neonatal rat ventricular myocytes (NRVMs)
100 nM
10 min
7,8-DHF increased ERK phosphorylation levels, similar to LM22A-4
Circ Res. 2023 Mar 31;132(7):867-881.
adult murine ventricular myocytes
2.5 μM, 5 μM, 10 μM
7,8-DHF dose-dependently increased sarcomere shortening and whole Ca2+ transient, similar to LM22A-4
Circ Res. 2023 Mar 31;132(7):867-881.
primary cortical neurons
500 nM
3 days
7,8-DHF significantly increased the total dendritic length and branching complexity of neurons.
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