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Bucladesine

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Mohammad Sharifzadeh – 1st expert on this subject based on the ideXlab platform

  • A cAMP analog attenuates beta-amyloid (1-42)-induced mitochondrial dysfunction and spatial learning and memory deficits.
    Brain Research Bulletin, 2018
    Co-Authors: Mehdi Aghsami, Mohammad Sharifzadeh, Mohammad Reza Sepand, Meysam Yazdankhah, Seyed Afshin Seyednejad, Jalal Pourahmad

    Abstract:

    Abstract Alzheimer’s disease (AD), a neurodegenerative disorder in elderly, is indicated with deposition of Amyloid β (Aβ) in the brain and accompanied with cognitive impairment. Bucladesine, a phosphodiesterase inhibitor, may ameliorate AD’s cognitive dysfunctions through mimicking the action of cAMP and raising its intracellular level. Here, we investigated the effects of Bucladesine on Aβ-induced memory and learning impairment in a Morris water maze (MWM) model. Rats were injected with Bucladesine (1 μl/side from a 100 μM stock solution) and Aβ (1 μl/side from a 100 μM stock solution) intra-hippocampally and after 19 days were trained for 4 successive days. The oxidative stress was evaluated through measurement of thiobarbituric acid (TBARS), thiol groups, and ferric reducing antioxidant power (FRAP). Effect of Aβ and its combination with Bucladesine on the mitochondrial function was assessed according to changes in the ROS generation, mitochondrial membrane potential (MMP), mitochondrial swelling, ATP/ADP ratio, mitochondrial outer membrane damage and cytochrome C release. Our results showed a significant elevation in TBARS level after administration of Aβ causing mitochondrial ROS generation, swelling, outer membrane damage, cytochrome C release and also lower thiol, FRAP, and MMP levels. Aβ-induced spatial memory impairment was prevented by pre-treatment with Bucladesine and the changed mitochondrial and biochemical indices upon treatment dose were improved. Taken together, we have obtained satisfactory results suggesting protecting effects of Bucladesine against the Aβ-mediated memory deficit and implying its plausible beneficial capacity as a therapeutic agent in oxidative stress-associated neurodegenerative diseases.

  • effect of Bucladesine pentoxifylline and h 89 as cyclic adenosine monophosphate analog phosphodiesterase and protein kinase a inhibitor on acute pain
    Fundamental & Clinical Pharmacology, 2017
    Co-Authors: Forouz Salehi, Seyedeh Yalda Seyedi, Mahshid Sadat Hosseinizare, Haleh Aghajani, Mohammad Sharifzadeh

    Abstract:

    : The aim of this study was to determine the effects of cyclic adenosine monophosphate (cAMP) and its dependent pathway on thermal nociception in a mouse model of acute pain. Here, we studied the effect of H-89 (protein kinase A inhibitor), Bucladesine (Db-cAMP) (membrane-permeable analog of cAMP), and pentoxifylline (PTX; nonspecific phosphodiesterase (PDE) inhibitor) on pain sensation. Different doses of H-89 (0.05, 0.1, and 0.5 mg/100 g), PTX (5, 10, and 20 mg/100 g), and Db-cAMP (50, 100, and 300 nm/mouse) were administered intraperitoneally (I.p.) 15 min before a tail-flick test. In combination groups, we injected the first and the second compounds 30 and 15 min before the tail-flick test, respectively. I.p. administration of H-89 and PTX significantly decreased the thermal-induced pain sensation in their low applied doses. Db-cAMP, however, decreased the pain sensation in a dose-dependent manner. The highest applied dose of H-89 (0.5 mg/100 g) attenuated the antinociceptive effect of Db-cAMP in doses of 50 and 100 nm/mouse. Surprisingly, Db-cAMP decreased the antinociceptive effect of the lowest dose of H-89 (0.05 mg/100 g). All applied doses of PTX reduced the effect of 0.05 mg/100 g H-89 on pain sensation; however, the highest dose of H-89 compromised the antinociceptive effect of 20 mg/100 g dose of PTX. Co-administration of Db-cAMP and PTX increased the antinociceptive effect of each compound on thermal-induced pain. In conclusion, PTX, H-89, and Db-cAMP affect the thermal-induced pain by probably interacting with intracellular cAMP and cGMP signaling pathways and cyclic nucleotide-dependent protein kinases.

  • Protective Effect of a cAMP Analogue on Behavioral Deficits and Neuropathological Changes in Cuprizone Model of Demyelination
    Molecular Neurobiology, 2015
    Co-Authors: Gelareh Vakilzadeh, Tahereh Ghadiri, Fariba Khodagholi, Marzieh Darvishi, Amir Ghaemi, Farshid Noorbakhsh, Ali Gorji, Mohammad Sharifzadeh

    Abstract:

    Multiple sclerosis (MS) is an inflammatory demyelinating disease that leads to neuronal cell loss. Cyclic AMP and its analogs are well known to decrease inflammation and apoptosis. In the present study, we examined the effects of Bucladesine, a cell-permeable analogue of cyclic adenosine monophosphate (cAMP), on myelin proteins (PLP, PMP-22), inflammation, and apoptotic, as well as anti-apoptotic factors in cuprizone model of demyelination. C57BL/6J mice were fed with chow containing 0.2 % copper chelator cuprizone or vehicle by daily oral gavage for 5 weeks to induce reversible demyelination predominantly of the corpus callosum. Bucladesine was administered intraperitoneally at different doses (0.24, 0.48, or 0.7 μg/kg body weight) during the last 7 days of 5-week cuprizone treatment. Bucladesine exhibited a protective effect on myelination. Furthermore, Bucladesine significantly decreased the production of interleukin-6 pro-inflammatory mediator as well as nuclear factor-κB activation and reduced the mean number of apoptotic cells compared to cuprizone-treated mice. Bucladesine also decreased production of caspase-3 as well as Bax and increased Bcl-2 levels. Our data revealed that enhancement of intracellular cAMP prevents demyelination and plays anti-inflammatory and anti-apoptotic properties in mice cuprizone model of demyelination. This suggests the modulation of intracellular cAMP as a potential target for treatment of MS.

Ali Roghani – 2nd expert on this subject based on the ideXlab platform

  • post training intrahippocampal infusion of nicotine Bucladesine combination causes a synergistic enhancement effect on spatial memory retention in rats
    European Journal of Pharmacology, 2007
    Co-Authors: Mohammad Sharifzadeh, Ali Roghani, Alireza Zamanian, Shervin Gholizadeh, Kaveh Tabrizian, Maryam Etminani, Siavash Khalaj, Mohammadreza Zarrindast

    Abstract:

    Abstract We previously had shown that bilateral intrahippocampal infusion of 1 μg nicotine (but not 0.5 μg dose) led to an improvement in spatial memory retention in the Morris water maze task in male rats. We also reported that a similar type of bilateral infusion of H89, a protein kinase AII (PKA II) inhibitor, caused a deficit in spatial memory retention. In the present study, we wished to test the hypothesis that intrahippocampal infusion of dibutyryl cyclic AMP (DB-cAMP also called Bucladesine), a membrane permeable selective activator of PKA, into the CA1 region can cause an improvement in spatial memory in this maze task. Indeed, bilateral infusion of 10 and 100 μM Bucladesine (but not 1 and 5 μM doses) led to a significant reduction in escape latency and travel distance (showing an improvement in spatial memory) compared to the control. Also, bilateral infusion of 0.5 μg nicotine or 1 μM Bucladesine alone did not lead to an improvement in spatial memory. However, such bilateral infusion of Bucladesine at 1 and 5 μM concentrations infused within minutes after 0.5 μg nicotine infusion improved spatial memory retention. Taken together, our data suggest that intrahippocampal Bucladesine infusions improve spatial memory retention in male rats and that Bucladesine can interact synergistically with nicotine to improve spatial memory.

  • Post-training intrahippocampal infusion of nicotine–Bucladesine combination causes a synergistic enhancement effect on spatial memory retention in rats
    European Journal of Pharmacology, 2007
    Co-Authors: Mohammad Sharifzadeh, Alireza Zamanian, Shervin Gholizadeh, Kaveh Tabrizian, Maryam Etminani, Siavash Khalaj, Mohammadreza Zarrindast, Ali Roghani

    Abstract:

    Abstract We previously had shown that bilateral intrahippocampal infusion of 1 μg nicotine (but not 0.5 μg dose) led to an improvement in spatial memory retention in the Morris water maze task in male rats. We also reported that a similar type of bilateral infusion of H89, a protein kinase AII (PKA II) inhibitor, caused a deficit in spatial memory retention. In the present study, we wished to test the hypothesis that intrahippocampal infusion of dibutyryl cyclic AMP (DB-cAMP also called Bucladesine), a membrane permeable selective activator of PKA, into the CA1 region can cause an improvement in spatial memory in this maze task. Indeed, bilateral infusion of 10 and 100 μM Bucladesine (but not 1 and 5 μM doses) led to a significant reduction in escape latency and travel distance (showing an improvement in spatial memory) compared to the control. Also, bilateral infusion of 0.5 μg nicotine or 1 μM Bucladesine alone did not lead to an improvement in spatial memory. However, such bilateral infusion of Bucladesine at 1 and 5 μM concentrations infused within minutes after 0.5 μg nicotine infusion improved spatial memory retention. Taken together, our data suggest that intrahippocampal Bucladesine infusions improve spatial memory retention in male rats and that Bucladesine can interact synergistically with nicotine to improve spatial memory.

Kaveh Tabrizian – 3rd expert on this subject based on the ideXlab platform

  • Interactive involvement of hippocampal cAMP/PKA and cyclooxygenase-2 signaling pathways in spatial learning in the Morris water maze.
    Folia Neuropathologica, 2020
    Co-Authors: Kaveh Tabrizian, Mahmoud Hashemzaei, Ali Akbar Nasiri, Sheyda Najafi, Fatemeh Amelinia, Mehdi Sanati, Farzaneh Shamshirgaran, Sahar Fanoudi

    Abstract:

    INTRODUCTION: Accumulated evidence shows that the cAMP-PKA signaling pathway plays a key role in memory functions. Cyclooxygenase-2, a critical player in neuroinflammation, has been confirmed in the pathogenesis of neurodegenerative diseases. This study is aimed to assess the effect of the interaction of cAMP-PKA and cyclooxygenase pathways on spatial memory acquisition in animal models. MATERIAL AND METHODS: In the present study, the effects of the four-day bilateral intra-hippocampal infusions of H-89 as a protein kinase AII inhibitor (10 µM/side), celecoxib (0.1 M/side) as a selective cyclooxygenase-2 inhibitor, cele-coxib/H-89 and Bucladesine (10 µM/side)/celecoxib/H-89 on spatial memory acquisition in the Morris water maze were investigated. Control animals received bilateral intra-hippocampal infusions of dimethyl sulfoxide. Rats were trained for 4 days; each day included one block of four trials. Post-training probe trial tests were performed on day five. RESULTS: A bilateral intra-hippocampal infusion of H-89 and celecoxib led to a significant impairment in spatial learning compared to the controls through a notable decrease in escape latency and traveled distance. But, combination treatment of animals with celecoxib/H-89 and Bucladesine/celecoxib/H-89 could considerably reverse celecoxib and H-89-induced spatial memory acquisition impairments in the Morris water maze. CONCLUSIONS: These results indicate the probable regulatory effects of cAMP/PKA and cyclooxygenase-2 signaling pathways on spatial memory acquisition in the Morris water maze.

  • Zinc Chloride and Lead Acetate-Induced Passive Avoidance Memory Retention Deficits Reversed by Nicotine and Bucladesine in Mice
    Biological Trace Element Research, 2016
    Co-Authors: Kaveh Tabrizian, Borna Payandemehr, Maryam Belaran, Mahmoud Hashemzaei, Mehdi Sanati, Abdolmajid Yazdani, Behnam Baheri, Abdolhossein Miri, Majid Zandkarimi, Sahar Fanoudi

    Abstract:

    It is very important to investigate the neurotoxic effects of metals on learning and memory processes. In this study, we tried to investigate the effects and time course properties of oral administration of zinc chloride (25, 50, and 75 mg/kg, for 2 weeks), lead acetate (250, 750, 1,500, and 2,500 ppm for 4, 6 and 8 weeks), and their possible mechanisms on a model of memory function. For this matter, we examined the intra-peritoneal injections of nicotine (0.25, 0.5, 1, and 1.5 mg/kg) and Bucladesine (50, 100, 300, and 600 nM/mouse) for 4 days alone and in combination with mentioned metals in the step-through passive avoidance task. Control animals received saline, drinking water, saline, and DMSO (dimethyl sulfoxide)/deionized water (1:9), respectively. At the end of each part of studies, animals were trained for 1 day in step-through task. The avoidance memory retention alterations were evaluated 24 and 48 h later in singular and combinational studies. Zinc chloride (75 mg/kg) oral gavage for 2 weeks decreased latency times compared to control animals. Also, lead acetate (750 ppm oral administrations for 8 weeks) caused significant lead blood levels and induced avoidance memory retention impairments. Four-days intra-peritoneal injection of nicotine (1 mg/kg) increased latency time compared to control animals. Finally, findings of this research showed that treatment with intra-peritoneal injections of nicotine (1 mg/kg) and/or Bucladesine (600 nM/mouse) reversed zinc chloride- and lead acetate-induced avoidance memory retention impairments. Taken together, these results showed the probable role of cholinergic system and protein kinase A pathways in zinc chloride- and lead acetate-induced avoidance memory alterations.

  • the quantitative evaluation of cholinergic markers in spatial memory improvement induced by nicotine Bucladesine combination in rats
    European Journal of Pharmacology, 2010
    Co-Authors: Kian Azami, Kaveh Tabrizian, Maryam Etminani, Fatemeh Salar, Maryam Belaran, Asieh Hosseini, Ali Hosseinisharifabad, Mohammad Sharifzadeh

    Abstract:

    Abstract We previously showed that post-training intra-hippocampal infusion of nicotine–Bucladesine combination enhanced spatial memory retention in the Morris water maze. Here we investigated the role of cholinergic markers in nicotine–Bucladesine combination-induced memory improvement. We assessed the expression of choline acetyltransferase (ChAT) and vesicular acetylcholine transporter (VAChT) in CA1 region of the hippocampus and medial septal area (MSA) of the brain. Post-training bilateral infusion of a low concentration of either nicotine or Bucladesine into the CA1 region of the hippocampus did not affect spatial memory significantly. Quantitative immunostaining analysis of optical density in CA1 regions and evaluation of immunopositive neurons in medial septal area of brain sections from all combination groups revealed a significant increase (P