Dibutyryl-cAMP, sodium salt, also known as Bucladesine, is a cell-permeable cyclic nucleotide analogue which mimics the action of endogenous cAMP and acts as a phosphodiesterase inhibitor[1]. Dibutyryl-cAMP, sodium salt is widely used to increase intracellular cAMP level[2] and is commonly employed in research on cell signaling, neurobiology, and inflammation[3].
Dibutyryl-cAMP, sodium salt (300nM; 1h) treatment can induce neuronal differentiation by up-regulating the expression of nur77, through the acetylation of Lys14 on histone H3 in PC12 cells[4]. Apoptosis induced by SGP in PC12 cells can be inhibited by 0.5mM to 1mM dibutyryl-cAMP, sodium salt[5].
Dibutyryl-cAMP, sodium salt (300nM/mouse; i.p.) pretreatment altered seizure parameters induced by pentylenetetrazol (PTZ), significantly decreasing seizure latency and threshold[6]. Dibutyryl-cAMP, sodium salt (50, 100, 300nM/mouse; i.p.) significantly decreased thermal-induced pain sensation in a dose-dependent manner in mice[7].
References:
[1]. Azami K, Etminani M, Tabrizian K, et al. The quantitative evaluation of cholinergic markers in spatial memory improvement induced by nicotine-bucladesine combination in rats. Eur J Pharmacol. 2010 Jun 25;636(1-3):102-7. doi: 10.1016/j.ejphar.2010.03.041. Epub 2010 Mar 31. PMID: 20361958.
[2]. Neumann S, Bradke F, Tessier-Lavigne M, et al. Regeneration of sensory axons within the injured spinal cord induced by intraganglionic cAMP elevation. Neuron. 2002 Jun 13;34(6):885-93. doi: 10.1016/s0896-6273(02)00702-x. PMID: 12086637.
[3]. Rundfeldt C, Steckel H, Sörensen T, Wlaź P. The stable cyclic adenosine monophosphate analogue, dibutyryl cyclo-adenosine monophosphate (bucladesine), is active in a model of acute skin inflammation. Arch Dermatol Res. 2012 May;304(4):313-7. doi: 10.1007/s00403-012-1216-6. PMID: 22302126; PMCID: PMC3332354.
[4]. Maruoka H, Sasaya H, Shimamura Y, et al. Dibutyryl-cAMP up-regulates nur77 expression via histone modification during neurite outgrowth in PC12 cells. J Biochem. 2010 Jul;148(1):93-101. doi: 10.1093/jb/mvq036. Epub 2010 Apr 7. PMID: 20375114.
[5]. Kobayashi Y, Shinozawa T. Effect of dibutyryl cAMP and several reagents on apoptosis in PC12 cells induced by a sialoglycopeptide from bovine brain. Brain Res. 1997 Dec 19;778(2):309-17. doi: 10.1016/s0006-8993(97)01072-x. PMID: 9459548.
[6]. Hosseini-Zare MS, Salehi F, Seyedi SY, et al. Effects of pentoxifylline and H-89 on epileptogenic activity of bucladesine in pentylenetetrazol-treated mice. Eur J Pharmacol. 2011 Nov 30;670(2-3):464-70. doi: 10.1016/j.ejphar.2011.09.026. Epub 2011 Sep 21. PMID: 21946102.
[7]. Salehi F, Hosseini-Zare MS, Aghajani H, Seyedi SY, Hosseini-Zare MS, Sharifzadeh M. Effect of bucladesine, pentoxifylline, and H-89 as cyclic adenosine monophosphate analog, phosphodiesterase, and protein kinase A inhibitor on acute pain. Fundam Clin Pharmacol. 2017 Aug;31(4):411-419. doi: 10.1111/fcp.12282. Epub 2017 Apr 26. PMID: 28267871.
Dibutyryl-cAMP, sodium salt，又称为Bucladesine，是一种细胞膜可透性环核苷酸类似物，能模拟内源性cAMP的作用，并作为磷酸二酯酶抑制剂[1]。Dibutyryl-cAMP, sodium salt广泛用于增加细胞内cAMP水平[2]，常用于细胞信号传导、神经生物学和炎症研究[3]。
Dibutyryl-cAMP, sodium salt (300nM; 1小时)处理可通过组蛋白H3上Lys14的乙酰化在PC12细胞中上调nur77的表达，从而诱导神经分化[4]。由SGP诱导的PC12细胞凋亡可被0.5mM至1mM的Dibutyryl-cAMP, sodium salt抑制[5]。
Dibutyryl-cAMP, sodium salt (300nM/mouse; 腹腔注射)预处理改变了戊四氮(PTZ)诱导的癫痫参数，显著减少了癫痫发作潜伏期和阈值[6]。Dibutyryl-cAMP, sodium salt (50, 100, 300nM/mouse，腹腔注射)以剂量依赖性方式显著减少了小鼠的热诱导疼痛感觉[7]。