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Minocycline

CAS No. : 10118-90-8

MCE 站：Minocycline

产品活性：Minocycline 是一种口服有效、能透过血脑屏障的半合成四环素类抗生素。Minocycline 是一种缺氧诱导因子 (HIF-1α) 抑制剂。Minocycline 具有抗癌(anti-cancer)，抗炎(anti-inflammatory) 和谷氨酸 (glutamate) 拮抗作用。Minocycline 降低谷氨酸神经传递，显示神经保护特性和抗抑郁作用。Minocycline 通过与细菌核糖体 30S 亚基结合，抑制细菌蛋白的合成，从而产生抑菌 (bacteriostatic) 作用。

研究领域：Anti-infection  |  Metabolic Enzyme/Protease  |  Apoptosis  |  Membrane Transporter/Ion Channel  |  Neuronal Signaling

作用靶点：Antibiotic  |  Bacterial  |  HIF/HIF Prolyl-Hydroxylase  |  Apoptosis  |  MDM-2/p53  |  Potassium Channel  |  Calcium Channel

In Vitro: Minocycline (0-100 μM, 24-72 h) suppresses proliferation ａnd clonogenic activity of ovarian cancer cell-lines (OVCAR-3, SKOV-3 ａnd A2780).
Minocycline (0-100 μM, 24-48 h)arrests cell cycle through inhibition of cyclins ａnd suppression of DNA incorporation.
Minocycline (0-100 μM, 72 h) induces cell apoptosis in ovarian cancer cell lines.
Minocycline shows direct neuronal protection, ａnd this mode of protection is likely to be associated with the preservation of mitochondrial integrity ａnd cytochrome c, followed by the suppression of caspase-dependent as well as caspase-independent cell death.
Minocycline leads to suppression of Hypoxia-inducible factor (HIF)-1α accompanied by up-regulation of p53 protein levels ａnd inactivation of AKT/mTOR/p70S6K/4E-BP1 pathway.

In Vivo: Minocycline (0-30 mg/kg, orally, daily for 4 weeks) suppresses OVCAR-3 tumor growth in female nude mice.
Minocycline (IP) is an effective neuroprotective agent in animal models of cerebral ischemia when given in high doses intraperitoneally.
Minocycline (0-40 mg/kg, IP, once) significantly attenuats METH-induced hyperlocomotion ａnd the development of behavioral sensitization in mice.
Minocycline (3 ａnd 10 mg/kg, IV, once) is effective at reducing infarct size in a Temporary Middle Cerebral Artery Occlusion model (TMCAO).
Minocycline (3-10 mg/kg, IV, once) results in serum levels (at 3 mg/kg) similar to that achieved in humans after a standard 200 mg dose.
Minocycline attenuates ischemia-induced ventricular arrhythmias in rats. This effect may be associated with activations of PI3K/Akt signaling pathway, mitochondrial KATP channels ａnd L-type Ca2+ channels.

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