6-Methoxyflavone is an orally active methoxyflavone. 6-Methoxyflavone suppresses neuroinflammation in microglia through the inhibition of TLR4/MyD88/p38 MAPK/NF-κB dependent pathways and the activation of HO-1/NQO-1 signaling. 6-Methoxyflavone induces S-phase arrest through the CCNA2/CDK2/p21CIP1 signaling pathway in HeLa cells. 6-Methoxyflavone inhibits NFAT Translocation into the nucleus and suppresses T cell activation. 6-Methoxyflavone partially restores chronic ethanol-induced behavioral deficits in mice. 6-Methoxyflavone antagonizes chronic constriction injury and diabetes associated neuropathic nociception expression. 6-Methoxyflavone can be used for the study of cancer, inflammation and neurological diseases[1][2][3][4][5].
细胞效力 (Cellular Effect)
Cell Line
Type
Value
Description
References
A2780 ADR
IC50
13 μM
Compound: 8
Inhibition of P-gp expressed in A2780adr cells by calcein AM accumulation assay
Inhibition of P-gp expressed in A2780adr cells by calcein AM accumulation assay
Suppressed LPS-induced phosphorylation of NF-κB p65 and IκB.
reduced LPS-induced expression of TLR4, MyD88 and phosphorylation of p38 MAPK, JNK.
Decreased iNOS and COX-2 expression.
Increased HO-1 and NQO1 expression.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Male BALB/c mice (22–28 g) were used, with chronic ethanol-induced cognitive impairment models established by oral administration of 25% w/v ethanol (2.0 g/kg daily) for 24 consecutive days, followed by 6 days of ethanol withdrawal[2]
Dosage:
25, 50, 75 mg/kg
Administration:
p.o. once daily 15 min before ethanol for 24 days
Result:
Restored locomotor activity suppressed by chronic ethanol and enhanced activity during abstinence and post-withdrawal.
Improved novel object recognition, with increased exploration time on days 12, 24, during abstinence, and post-withdrawal.
Enhanced Morris water maze performance.
Ameliorated Y-maze deficits and enhanced nest-building.
Increased socialization, with all doses raising exploration time with novel juveniles at all stages.
Raised frontal cortical dopamine and vitamin C and reversed frontal cortical noradrenaline reduction.
Increased hippocampal dopamine and elevated hippocampal noradrenaline.
Animal Model:
3-month-old male C57BL/6 mice were used, with LPS-induced brain inflammatory models established by intraperitoneal injection of LPS (5 mg/kg) 3 h before sacrifice, following pretreatment with 6-methoxyflavone or PBS for 4 days[3]
Dosage:
25, 50 mg/kg
Administration:
i.p. once daily for 4 days before LPS injection 3 h prior to sacrifice
Result:
Reduced microglial cell density in the prefrontal cortex (PFC) and substantia nigra (SN) after LPS stimulation.
Decreased cell size of Iba1-positive microglia in PFC and SN, with 50 mg/kg showing significant effects.
Increased cell process length of microglia in PFC and SN, improving morphological abnormalities induced by LPS.
Suppressed phosphorylation of p38 in PFC and SN, inhibiting overactivation of the p38 MAPK signaling pathway.
Reduced MyD88 protein expression in SN, downregulating the TLR4/MyD88 dependent pathway.
Animal Model:
Sprague-Dawley rats (male, 300-450 g) were used, with CCI-induced mononeuropathy models established by exposing the sciatic nerve and applying four double knot ligatures (1 mm apart) prior to its trifurcation[4]
Dosage:
25, 50, 75 mg/kg
Administration:
i.p. once daily for 21 days
Result:
Reduced static mechanical allodynia, as evidenced by increased paw withdrawal threshold to von Frey filaments in the operated hindpaw.
Alleviated dynamic mechanical allodynia, shown by prolonged paw withdrawal latency to light brushing with a cotton bud.
Attenuated heat hyperalgesia.
Diminished cold allodynia.
Relieved pin-prick hyperalgesia.
Improved locomotor activity.
Enhanced motor coordination.
Showed normal gait, reflected by reduced overlap distance between forepaw and hindpaw placement in footprint analysis.
Animal Model:
Sprague-Dawley rats (female, 180-220 g) were used, with STZ-induced diabetic polyneuropathy models established by a single intraperitoneal injection of streptozotocin (50 mg/kg) after 16 h fasting, and rats with random blood glucose levels exceeding 250 mg/dL 72 h post-injection were included in the experiment[4]
Dosage:
25, 50, 75 mg/kg
Administration:
i.p. once daily for 21 days
Result:
Reduced static mechanical allodynia in bilateral hindpaws.
Alleviated dynamic mechanical allodynia in bilateral hindpaws.
Attenuated heat hyperalgesia in bilateral hindpaws.
Relieved static mechanical vulvodynia.
Alleviated dynamic mechanical vulvodynia.
Improved locomotor activity.
Enhanced motor coordination.
Showed normal gait, shown by reduced overlap distance between forepaw and hindpaw placement in footprint analysis.
Animal Model:
BALB/c mice were used, with experimental atopic dermatitis models established by stripping the ear surface five times with surgical tape, painting with 20 μL 4% 2,4-dinitrochlorobenzene (dissolved in acetone/olive oil solution at a 1:3 ratio) for sensitization, and then challenging the ears with 20 μL 2% dinitrochlorobenzene and 20 μL dust mite extracts (10 mg/mL) dissolved in PBS containing 0.5% Tween 20 once per week for 6 weeks[5]
Dosage:
20, 100 mg/kg
Administration:
i.g. five times per week for 6 weeks
Result:
Reduced infiltration of lymphocytes in the ears.
Decreased thickness of the epidermis.
Lowered serum IgE levels.
Ameliorated symptoms such as erythema, horny substance, dryness, and scaling.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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