3′,4′,7-Trihydroxyflavone

3′,4′,7-Trihydroxyflavone is an orally active inhibitor of OXA-48 (IC₅₀ = 1.89 μM) and COX-1 (IC₅₀ = 36.37 μM). 3′,4′,7-Trihydroxyflavone exhibits antioxidant and anti-inflammatory properties, inhibiting the release of inflammatory cytokines such as IL-6, IL-8, and TNF-α. 3′,4′,7-Trihydroxyflavone inhibits H₂O₂-induced neuronal apoptosis and ROS accumulation, and exerts anti-neuroinflammatory effects by suppressing the JNK-STAT1 pathway. 3′,4′,7-Trihydroxyflavone exhibits antimicrobial and antibiotic-modifying activities against multidrug-resistant Gram-negative enteric bacteria. 3′,4′,7-Trihydroxyflavone inhibits RANKL-induced osteoclast formation via NFATc1. 3′,4′,7-Trihydroxyflavone activates the CREB-BDNF axis and restores scopolamine (HY-N0296)-induced memory deficits in mice^{[1][2][3][4][5][6][7][8][9]}. In Vitro:3′,4′,7-Trihydroxyflavone (0.1-20 μM, 24 h) enhances the cell viability and survival against Scopolamine (HY-N0296)-induced damage in SH-SY5Y cells^[1].
3′,4′,7-Trihydroxyflavone (0.1-100 µM) reduces the secretion of IL-6 and IL-8 in TNFα-stimulated HaCaT cells, with IC₅₀s of 17.8, 126.2 µg/mL, with maximum inhibition rates of 74.4, 40.2 %, reduces HaCaT cell viability to 74%^[2].
3′,4′,7-Trihydroxyflavone (50 µM, 64 μg/mL) inhibits OXA-48 activity by 80% and exhibits antimicrobial activity against BW25113 ∆acrA∆bamB (OXA-48) in combination with β-lactam antibiotics^[3].
3′,4′,7-Trihydroxyflavone (1-20 μM, 30 min) prevents H₂O₂-induced cell death and lactate dehydrogenase (LDH) release in SH-SY5Y and hippocampal neuronal cells^[4].
3′,4′,7-Trihydroxyflavone (1-20 µM, 30 min) inhibits H₂O₂-induced apoptotic features of SH-SY5Y cells, reverses induced nuclear necrosis, and condenses cell shrinkage^[4].
3′,4′,7-Trihydroxyflavone (0.5-20 µM, 30 min) inhibits H₂O₂-induced ROS accumulation, SOD, CAT, and GSH reduction, and activation of F-κB p65 translocation from the cytosol to the nucleus in SH-SY5Y cells^[4].
3′,4′,7-Trihydroxyflavone (1-20 µM, 30 min) inhibits H₂O₂-induced phosphorylation of JNK, p38, ERK 1/2 MAPKs and PI3K/Akt levels, upregulation of Bax, caspase-3, caspase-9 and PARP levels, downregulation of Bcl-2 and Bcl-xL levels, release of cytochrome c and loss of MMP in SH-SY5Y cells^[4].
3′,4′,7-Trihydroxyflavone shows antibacterial activity against 12 Gram-negative bacteria E. coli, E. aerogenes, K. pneumonia, with MIC values ranging from 4 to 256 μg/mL^[5].
3′,4′,7-Trihydroxyflavone improves the activity of Tetracycline (HY-A0107) and Erythromycin (HY-B0220) on 80% of the tested bacteria, with FIC values ranging from 0.5 to < 0.062^[5].
3′,4′,7-Trihydroxyflavone (0.1-100 μM) has no effect at 0.1–30 µM, but decreases cell viability at 100 µM for MG6 cells^[6].
3′,4′,7-Trihydroxyflavone (0.1-10 μM, 6-48 h) reduces NO, TNF-α, and iNOS levels, inhibits STAT1 phosphorylation and total STAT1 expression in LPS (HY-D1056)-induced MG6 cells^[6].
3′,4′,7-Trihydroxyflavone (0.1-10 μM, 0.5 h) inhibits JNK phosphorylation but not p38 or ERK phosphorylation in LPS-induced MG6 cells^[6].
3′,4′,7-Trihydroxyflavone (0.1-10 μM, 24-48 h) inhibits NO release, iNOS expression, STAT1 phosphorylation in IFN-γ-induced MG6 cells^[6].
3′,4′,7-Trihydroxyflavone (0-5 μg/mL, 1-7 days) inhibits RANKL-induced osteoclast formation and bone resorption in BMMs^[7].
3′,4′,7-Trihydroxyflavone (5 μg/mL, 7 days) suppresses RANKL-induced NFATc1 expression via Blimp-1 and p38 MAPK pathway in BMMs^[7].
In Vivo:3′,4′,7-Trihydroxyflavone (10/50 mg/kg, p.o., once a day, 3 days/three times per week, 28 days; 10 ng, ICV, twice a week, 28 days) plays a neuroprotective role by inducing CREB-BDNF activation, improving long-term potentiation (LTP) in Scopolamine-induced cognitive deficits mice model^[1].