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  5. Aspirin lithium

Aspirin lithium  (Synonyms: Acetylsalicylic acid lithium; ASA lithium)

目录号: HY-14654A
产品使用指南 技术支持

Aspirin (Acetylsalicylic Acid) lithium 是一种口服有效的不可逆的环氧合酶 COX-1COX-2 抑制剂,IC50 分别为 5 和 210 μg/mL. Aspirin lithium 诱导细胞凋亡 (apoptosis)。Aspirin lithium 可抑制 NF-κB 的活化。Aspirin lithium 还抑制血小板前列腺素合成酶 (prostaglandin synthetase),可预防冠状动脉和脑血管血栓形成。

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Aspirin lithium

Aspirin lithium Chemical Structure

CAS No. : 552-98-7

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Aspirin lithium 的其他形式现货产品:

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MCE 顾客使用本产品发表的 29 篇科研文献

WB

    Aspirin lithium purchased from MCE. Usage Cited in: Cell Death Dis. 2018 Aug 28;9(9):847.  [Abstract]

    HIPK2 expression is upregulated by treatments with 5 μM Resveratrol, 30 μM Aspirin, 10 μM Vitamin E, and 15 μM Ursolic acid for another 16 h after the LPS treatment, as analysed by western blotting.
    • 生物活性

    • 纯度 & 产品资料

    • 参考文献

    生物活性

    Aspirin (Acetylsalicylic Acid) lithium is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin lithium induces apoptosis. Aspirin lithium inhibits the activation of NF-κB. Aspirin lithium also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis[1][2][3][4][5][6].

    IC50 & Target

    COX-1

     

    COX-2

     

    体外研究
    (In Vitro)

    Aspirin lithium 抑制人关节软骨细胞中的 COX-1COX-2,IC50 值分别为 3.57 μM 和 29.3 μM[2]
    Aspirin acetylates COX-1 的丝氨酸 530,从而阻断血小板中血栓素 A 的合成,减少血小板聚集[3]
    Aspirin lithium 通过干扰 CCAAT/增强子结合抑制 COX-2 蛋白表达蛋白质 beta (C/EBPbeta) 与其在 COX-2 启动子/增强子上的同源位点[3]
    Aspirin lithium 抑制 NF-κB 依赖性转录自 lgκ 增强子和人类免疫缺陷病毒 (HIV) 转染 T 细胞中的长末端重复序列 (LTR)[4]
    Aspirin lithium 通过激活半胱天冬酶、激活 p38 MAP 激酶、释放线粒体细胞色素 c、和神经酰胺途径的激活[6]

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    体内研究
    (In Vivo)

    注意
    请勿仅参考一篇文章来确定实验条件。建议在正式实验前,通过预实验确定最佳实验条件 (动物品系、年龄、剂量、频率及周期、检测时间及指标等)。

    Aspirin lithium (5-150 mg/kg,口服,一次) 对成年酵母菌发热雄性大鼠表现出显著的解热活性[2]
    Aspirin 可用于诱导胃肠溃疡模型[8]

    诱导胃肠溃疡模型[8]
    致病原理
    Aspirin 可抑制动物内源性前列腺素(PG)的合成。Aspirin 还能溶解粘膜上皮细胞的磷脂,导致粘膜通透性增加。
    具体造模方法:
    小鼠:白化病小鼠 • 雄性 • 6 周龄
    给药方式:500 mg/kg • oral • 单剂量
    造模成功指标
    组织学改变: 造成表皮上皮细胞的侵蚀。
    导致粘膜厚度减少。
    无COX-1反应诱发溃疡。
    相关产品:/
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    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Model: Male albino Charles River rats (200-250 g, 8 animals/group, fever was induced by 20 mL/kg of a 20% aqueous suspension of brewer’s yeast which was injected SC in the back below the nape of the neck)[7]
    Dosage: 5, 25, 50, 100 and 150 mg/kg
    Administration: PO, once
    Result: Produced a statistically significant decrease of 0.23°C at 15 min post-drug at the dose of 150 mg/kg. Antipyretic effect gradually increased in magnitude until a peak effect of 1.96 °C was reached at 120 min post-drug. The ED50 of aspirin was found to be 10.3 mg/kg with confidence limits of 1.8-23.0 mg/kg. The antipyretic response to aspirin is dependent on the dose of the compound administered.
    Animal Model: Albino male mice [8]
    Dosage: 500 mg/kg, single dose
    Administration: oral
    Result: Caused erosion of the surface epithelial cells.
    Resulted in a decrease in the mucosal thickness.
    Induced ulcer without COX-1 reaction.
    Clinical Trial
    分子量

    186.09

    Formula

    C9H7LiO4

    CAS 号
    运输条件

    Room temperature in continental US; may vary elsewhere.

    储存方式

    Please store the product under the recommended conditions in the Certificate of Analysis.

    纯度 & 产品资料
    参考文献
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    • Do most proteins show cross-species activity?

      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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    目录号:
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