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/布拉地新钠盐 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Hepatocyte couplets
10 µM
30 min
To study the protective effect of DBcAMP against TLC-induced cholestasis, results showed DBcAMP significantly improved cVA of CLF
Gut. 2002 Jul;51(1):113-9.
oligodendrocyte progenitor cells (OPCs)
3.21 mM
48 h
dbcAMP promotes OPC differentiation in the presence of myelin-associated inhibitors, increasing O4 and Mbp expression
EMBO Mol Med. 2013 Dec;5(12):1918-34
L6 cells
1mM
2.5h
To test the effect of DBcAMP on glucose uptake (GU). Results showed that DBcAMP significantly increased GU.
Systemic administration of Cyclic AMP and IL-4 after spinal cord injury significantly promotes M1 to M2a phenotypic conversion and reduces inflammatory responses.
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