PKA is a ubiquitous cellular kinase, also known as cAMP-dependent protein kinase (cAMP), and it is well-established that plays an important role in regulating several functions of cell processes, including regulation of glycogen, sugar, and lipid metabolism[3]. Dibutyryl-cAMP is a cell-permeable PKA activator that functions by preferentially activating endogenous cAMP. In vitro assays, Dibutyryl-cAMP was found to significantly suppress TNF-a production in a dose-dependent manner, with IC50 values of 247, 28.9, and 25.4 μM, respectively in RAW264.7 cells[4]. Additionally, rat hepatocytes were cultured with cAMP agonists dibutyryl-cAMP inhibits Nitric oxide synthesis and inducible nitric oxide synthase (iNOS) expression through effects on the iNOS promoter region and NF-kB-binding activity[5]. In hepatocytes, Dibutyryl-cAMP can prevent tumor necrosis factor α plus acti-nomycin D (TNFα/ActD)-induced apoptosis via a PKA-dependent mechanism[6]. In vivo model, Dibutyryl-cAMP showed a distinct anti-fibrotic effect via PKA/p-CREB/CBP signaling. Treatment of Dibutyryl-cAMP resulted in the decrease of the number and size of silicosis nodules, inhibition of myofibroblast differentiation, and extracellular matrix deposition[7]. Moreover, 4 days intra-peritoneal injections of bucladesine (600 nM/mouse) significantly reversed zinc chloride- and led acetate-induced avoidance memory retention alterations compared to control animals[8].
Bucladesine sodium 细胞研究
细胞系
浓度
检测类型
检测时间
活动说明
数据源
mouse RAW264.7 cells
Function assay
4 h
Antiinflammatory activity against mouse RAW264.7 cells assessed as inhibition of LPS-induced TNFalpha production after 4 hrs by ELISA, IC50=28.9 μM
11000020
mouse S49 cells
500 μM
Cytotoxicity assay
20-49 h
Cytotoxicity against HGPRTase-deficient mouse S49 cells assessed as growth inhibition at 500 uM after 20 to 49 hrs by time-course study
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