生物活性 | |||
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描述 | Acacetin is an orally active flavonoid derived from Tephroseris kirilowii (Turcz.) Holub. Acacetin (10-200 μM; 24 hours) decreases cell viabilities in a dose-dependent manner. Acacetin has little effect on human normal glial cell line HEB and non-tumorigenic epithelial cell line MCF-10A. Acacetin (50-150 μM; 24 hours) causes G2/M cell cycle arrest and induces apoptosis and autophagy and leads to decreases in levels of PI3Kγ-p110, p-AKT, p-mTOR, p-p70S6K, and p-ULK in a dose-dependent manner[3]. Acacetin significantly inhibited the release of NO and prostaglandin E(2) and the expression of inducible NO synthase and cyclooxygenase-2 in LPS-stimulated BV-2 cells. The compound also reduced proinflammatory cytokines, TNF-α and IL-1β, and inhibited the activation of NF-κB and p38 MAPK[4]. The natural compound, acacetin, inhibits glutamate release from hippocampal synaptosomes by attenuating voltage-dependent Ca(2+) entry and effectively prevents KA-induced in vivo excitotoxicity[5]. Acacetin (1.8-56.2 mg/kg/day; ip; single dose) decreases visceral and inflammatory nociception and prevented the formalin-induced oedema[4]. Chronic acatetin (5, 15 or 45 mg/kg, p.o., once per day for three weeks) administration to mice engenders antidepressant-like efficacy on both behavior and stress axis responsivity, with serotonergic system that preferentially couples with 5-HT1A receptors being critically involved. In vitro, acacetin (1-100 nM) increased the Emax of 8-OH-DPAT[6]. Intravenous infusion of acacetin prodrug (3, 6 and 12 mg/kg) terminated experimental AF without increasing ECG QTc interval in beagle dogs. The intravenous LD50 of acacetin prodrug was 721 mg/kg in mice[7]. |
实验方案 | |||
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1mg | 5mg | 10mg | |
1 mM 5 mM 10 mM |
3.52mL 0.70mL 0.35mL |
17.59mL 3.52mL 1.76mL |
35.18mL 7.04mL 3.52mL |
参考文献 |
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