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  • Singh, Nirmal  (433)
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  • 1
    Language: English
    In: Pharmacology, Biochemistry and Behavior, Sept, 2014, Vol.124, p.27(9)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.pbb.2014.05.002 Byline: Gurpreet Singh, Bhupesh Sharma, Amteshwar Singh Jaggi, Nirmal Singh Abstract: The study was designed to investigate the efficacy of bosentan a dual endothelin (ET.sub.A and ET.sub.B) receptor antagonist in experimental diabetes induced vascular endothelial dysfunction and associated dementia. Diabetes was induced in rats by administration of a single dose (50mg/kg, i.p.) of streptozotocin (STZ). Drug treatment was started after 1month of STZ administration and treatment was continued until the end of the study. Morris water maze (MWM) test was employed for testing spatial learning and memory. Endothelial function was measured on isolated aortic rings using student physiograph. Serum glucose, body weight, serum nitrite/nitrate, brain thiobarbituric acid reactive species (TBARS), reduced glutathione (GSH) levels, and brain acetylcholinesterase activity were also tested. STZ treatment resulted in significant development of cognitive and vascular endothelial deficits, manifested in the terms of endothelial dysfunction, impairment of learning and memory, reduction in body weight and serum nitrite/nitrate levels along with increase in serum glucose, brain acetylcholinesterase activity, TBARS, and decreased GSH levels. Treatment of bosentan attenuated diabetes induced impairment of learning, memory, endothelial function, and various biochemical parameters. It may be concluded that bosentan has shown efficacy in STZ induced cognitive and vascular endothelial deficits. Thus, endothelin receptors can be considered as a potential pharmacological target for the management of experimental diabetes induced vascular endothelial dysfunction and associated dementia. Article History: Received 5 February 2013; Revised 1 May 2014; Accepted 8 May 2014
    Keywords: Endothelin ; Glucose Metabolism ; Dementia ; Diabetes Mellitus ; Glucose ; Endothelium
    ISSN: 0091-3057
    Source: Cengage Learning, Inc.
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  • 2
    Language: English
    In: Psychopharmacology, June 15, 2011, Vol.215(4), p.677(11)
    Description: Rationale Vascular dementia is the second leading cause of dementia, which is strongly associated with diabetes. Diabetes and dementia have become a major public health concern worldwide. At this point of time, it is very important to find the possible pharmacological agents which may be useful in management and therapy of dementia including Alzheimer's disease, vascular dementia, etc. Objectives To investigate the effect of sodium butyrate on streptozotocin (STZ) diabetes induced vascular dementia in rats. Methods Diabetes and subsequent endothelial dysfunction and dementia were induced in rats by administration of single dose of STZ. Drug treatment was started after 1 month of STZ administration and treatment was continued until the end of the study. Morris water maze (MWM) test was employed for testing learning and memory. Endothelial function was measured on isolated aortic rings using student physiograph. Serum glucose, body weight, serum nitrite/nitrate, aortic superoxide anion generation, brain thiobarbituric acid reactive species (TBARS), reduced glutathione (GSH) levels, and acetylcholinesterase activity were also tested. Results STZ treatment produced endothelial dysfunction, impairment of learning and memory, reduction in body weight and serum nitrite/nitrate, and increase in serum glucose, aortic and brain oxidative stress (increased superoxide anion, TBARS, and decreased GSH levels), and brain acetylcholinesterase activity. Treatment of sodium butyrate attenuated diabetes induced impairment of learning, memory, endothelial function, and various biochemical parameters. Conclusions Sodium butyrate may be considered as potential pharmacological agent for the management of diabetes induced vascular dementia. Keywords Alzheimer * Dementia * Diabetes * HDAC * Endothelial dysfunction * Streptozotocin * Morris water maze * Nitrite/nitrate * Oxidative stress * Acetylcholinesterase activity
    Keywords: Streptozocin ; Glucose Metabolism ; Esters ; Vascular Dementia ; Superoxides ; Diabetes Mellitus ; Amyloid Beta-Protein ; Glucose ; Public Health ; Alzheimer'S Disease
    ISSN: 0033-3158
    Source: Cengage Learning, Inc.
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  • 3
    Language: English
    In: Psychopharmacology, 2012, Vol.223(3), pp.307-317
    Keywords: Nuclear factor kappa-B ; Angiotensin converting enzyme ; Endothelial dysfunction ; Morris water maze ; Alzheimer’s disease ; Oxidative stress
    ISSN: 0033-3158
    E-ISSN: 1432-2072
    Source: Springer Science & Business Media B.V.
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  • 4
    Language: English
    In: Physiology & Behavior, 01 June 2011, Vol.103(3-4), pp.321-329
    Description: The present study was designed to investigate whether adaptogenic factors may be transferred from stress adapted rats to naïve rats and to explore the nature of endogenous adaptogens by pharmacological modulation. The rats were subjected to cold water immersion stress by placing them individually in a tank of water (depth = 15.5 cm; temperature = 16 ± 2 °C) for 5 min. The rats were subjected to single episode of cold water immersion stress for acute stress; while for adaptation, the rats were subjected to repeated episodes of same stressor for 5 consecutive days. The plasma of stress adapted rats was administered to naïve rats before subjecting to acute stress. The stress related behavioral alterations were assessed using the actophotometer, the hole board, the open field and the social interaction tests. Acute stress with single episode of cold water immersion was associated with behavioral alterations. However, the behavioral alterations were significantly restored on subjecting repeated episodes of cold water immersion. Administration of plasma of stress adapted rats also attenuated acute stress associated behavioral alterations. Administration of naltrexone abolished the restoration of behavioral changes as a part of adaptive process in repeated stress subjected rats as well as the anti-stress effects of plasma of stress adapted rat. It may be concluded that opioids may be the potential endogenous adaptogens that tend to restore the homeostasis during repeated episodes of stress. Furthermore, the endogenous adaptogens may be transferred in the form of plasma from repeated stress subjected rats to the naïve rats to confer the anti-stress properties. ►Pharmacological studies on adaptation in cold water immersion stress subjected rats. ►Opioids may be the potential endogenous adaptogens. ►Plasma of stress adapted rat confers anti-stress activities.
    Keywords: Cold Water Immersion Stress ; Adaptation ; Opioids ; Behavior ; Anatomy & Physiology ; Psychology
    ISSN: 0031-9384
    E-ISSN: 1873-507X
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  • 5
    Language: English
    In: Bioorganic & Medicinal Chemistry, 01 February 2012, Vol.20(3), pp.1175-1180
    Description: Acetylcholinesterase (AChE) enzyme inhibition is an important target for the management of Alzheimer disease (AD) and AChE inhibitors are the main stay drugs for its management. Coumarins are the phytochemicals with wide range of biological activities including AChE inhibition. The scientists have attempted to explore the coumarin template for synthesizing novel AChE inhibitors with additional pharmacological activities including decrease in beta-amyloid (Aβ) deposition and beta-secretase inhibition that are also important for AD management. Most of the designed schemes have involved incorporation of a catalytic site interacting moiety at 3- and 4-positions of the coumarin ring. The present review describes these differently synthesized coumarin derivatives as AChE inhibitors for management of AD.
    Keywords: Acetylcholinesterase Inhibitor ; Alzheimer Disease ; Coumarin ; Benzylamino ; Medicine ; Chemistry ; Anatomy & Physiology
    ISSN: 0968-0896
    E-ISSN: 1464-3391
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  • 6
    Language: English
    In: European Journal of Pharmacology, 2010, Vol.648(1), pp.102-109
    Description: The present study was designed to investigate the ameliorative potential of spironolactone in chronic constriction injury and vincristine-induced neuropathic pain in rats. The chronic constriction injury was induced by placing four loose ligatures around the sciatic nerve, while vincristine (50 μg/kg) was administered for 10 days to induce chemotherapy-induced neuropathic pain. Acetone drop, pin-prick, hot plate and paint brush tests were performed to assess cold allodynia; mechanical and heat hyperalgesia; dynamic mechanical allodynia, respectively. The spontaneous pain and postural index in terms of foot deformity was also assessed. The levels of TNF-α were measured in the sciatic nerve as an index of inflammation. Chronic constriction injury led to significant development of cold allodynia; mechanical and heat hyperalgesia; dynamic mechanical allodynia; spontaneous pain and foot deformity along with rise in the levels of TNF-α. Administration of vincristine was associated with the development of allodynia and hyperalgesia without spontaneous pain, foot deformity and elevation in the levels of TNF-α. Administration of spironolactone (10 and 20 mg/kg) significantly attenuated chronic constriction injury-induced pain related behaviour and foot deformity along with attenuation of TNF-α levels, without modulating vincristine-induced neuropathic pain. The attenuating effect of spironolactone in chronic constriction injury may be due to its anti-inflammatory properties and ability to decrease pro-inflammatory cytokines, while involvement of non-inflammatory mechanisms in the pathogenesis of vincristine-induced pain may probably explain its lack of beneficial effect in chemotherapy associated pain.
    Keywords: Chronic Constriction Injury ; Vincristine ; Sciatic Nerve Ligation ; Spironolactone ; Inflammation ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0014-2999
    E-ISSN: 1879-0712
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  • 7
    Language: English
    In: Psychopharmacology, 2012, Vol.220(2), pp.427-438
    Description: Rationale Recently, nuclear factor kappa B is indicated in the precipitation of opioid withdrawal syndrome. NF-[kappa]B activation is noted to control the transcription and biochemical activation of chemokines. Opioid receptor activation-linked chemokine stimulation is reported to mediate certain effects produced by prolonged opioid treatment. Ammonium pyrrolidine dithiocarbamate (APD) and RS 102895 are relatively selective inhibitors of NF-[kappa]B and C-C chemokine receptor 2, respectively. Objectives The present study investigates the effect of APD and RS 102895 on morphine withdrawal signs in vitro and in vivo. Materials and methods Morphine was administered twice daily for 5 days, following which a single day 6 injection of naloxone (8 mg/kg, i.p.) precipitated opioid withdrawal syndrome in mice. Withdrawal syndrome was quantitatively assessed in terms of withdrawal severity score and the frequency of jumping, rearing, fore paw licking and circling. Naloxone-induced contraction in morphine-withdrawn isolated ratileum wasemployed asaninvitromodel. Anisobolographic study design was employed in the two models to assess potential synergistic activity between APD and RS 102895. Results APD and RS 102895 dose-dependently attenuated naloxone-induced morphine withdrawal syndrome both in vivo and in vitro. APD was also observed to exert a synergistic interaction with RS 102895. Conclusions It is concluded that APD and RS 102895 attenuate morphine withdrawal signs possibly by a NF-[kappa]B and C-C chemokine receptor 2 activation pathway-linked mechanisms potentially in an interdependent manner. Keywords Morphine dependence * Withdrawal syndrome * Nuclear factor kappa beta * C-C chemokine receptor 2
    Keywords: Morphine dependence ; Withdrawal syndrome ; Nuclear factor kappa beta ; C-C chemokine receptor 2
    ISSN: 0033-3158
    E-ISSN: 1432-2072
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  • 8
    Language: English
    In: Psychopharmacology, 2011, Vol.215(4), pp.677-687
    Description: Byline: Bhupesh Sharma (1), Nirmal Singh (1) Keywords: Alzheimer; Dementia; Diabetes; HDAC; Endothelial dysfunction; Streptozotocin; Morris water maze; Nitrite/nitrate; Oxidative stress; Acetylcholinesterase activity Abstract: Rationale Vascular dementia is the second leading cause of dementia, which is strongly associated with diabetes. Diabetes and dementia have become a major public health concern worldwide. At this point of time, it is very important to find the possible pharmacological agents which may be useful in management and therapy of dementia including Alzheimer's disease, vascular dementia, etc. Objectives To investigate the effect of sodium butyrate on streptozotocin (STZ) diabetes induced vascular dementia in rats. Methods Diabetes and subsequent endothelial dysfunction and dementia were induced in rats by administration of single dose of STZ. Drug treatment was started after 1 month of STZ administration and treatment was continued until the end of the study. Morris water maze (MWM) test was employed for testing learning and memory. Endothelial function was measured on isolated aortic rings using student physiograph. Serum glucose, body weight, serum nitrite/nitrate, aortic superoxide anion generation, brain thiobarbituric acid reactive species (TBARS), reduced glutathione (GSH) levels, and acetylcholinesterase activity were also tested. Results STZ treatment produced endothelial dysfunction, impairment of learning and memory, reduction in body weight and serum nitrite/nitrate, and increase in serum glucose, aortic and brain oxidative stress (increased superoxide anion, TBARS, and decreased GSH levels), and brain acetylcholinesterase activity. Treatment of sodium butyrate attenuated diabetes induced impairment of learning, memory, endothelial function, and various biochemical parameters. Conclusions Sodium butyrate may be considered as potential pharmacological agent for the management of diabetes induced vascular dementia. Author Affiliation: (1) Pharmacology Division, Department of Pharmaceutical Sciences and Drug Research, Faculty of Medicine, Punjabi University, Patiala, 147002, Punjab, India Article History: Registration Date: 03/01/2011 Received Date: 06/07/2010 Accepted Date: 31/12/2010 Online Date: 12/01/2011
    Keywords: Alzheimer ; Dementia ; Diabetes ; HDAC ; Endothelial dysfunction ; Streptozotocin ; Morris water maze ; Nitrite/nitrate ; Oxidative stress ; Acetylcholinesterase activity
    ISSN: 0033-3158
    E-ISSN: 1432-2072
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  • 9
    Language: English
    In: Brain Research, 24 March 2011, Vol.1381, pp.187-201
    Description: Neuropathic pain has been described as the “most terrible of all tortures which a nerve wound may inflict” and arises as a consequence of nerve injury either of the peripheral or central nervous system. Following peripheral nerve injury, a cascade of events in the primary afferents leads to peripheral sensitization resulting in spontaneous nociceptor activity, decreased threshold and increased response to supra-threshold stimuli. A series of molecular changes in spinal cord and brain centers are associated with central sensitization which is responsible for the pain to non-injured extra-territory regions (extraterritorial pain) and contralateral parts (mirror-image pain). The peripheral nerve injury has been reported to induce neuroplastic changes in different brain regions including the anterior cingulate cortex, insular cortex, ventrolateral orbitofrontal area, amygdala, striatum, thalamus, hypothalamus, rostral ventromedial medulla, periaqueductal gray, pons (locus coeruleus), red nucleus, and medulla oblongata. The present review article discusses the involvement of these different brain areas in the development of peripheral nerve injury-induced neuropathic pain.
    Keywords: Peripheral Nerve Injury ; Rostral Ventromedial Medulla ; Periaqueductal Gray ; Locus Coeruleus ; Hypothalamus ; Neuropathic Pain ; Anatomy & Physiology
    ISSN: 0006-8993
    E-ISSN: 1872-6240
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  • 10
    Language: English
    In: Pharmacology, Biochemistry and Behavior, December 2011, Vol.100(2), pp.320-329
    Description: Vascular dementia (VaD) is the second most common dementing illness. We have recently reported that diabetes induces VaD in rats. The present study has been designed to investigate the potential of peroxisome-proliferator-activated receptors-gamma (PPAR-γ) agonists in diabetes induced VaD of Wistar Albino rats. The rats were administered, single dose of streptozotocin (STZ) for the induction of diabetes. Morris water-maze (MWM) test was employed for testing learning and memory. Serum glucose, bodyweight, vascular endothelial function, serum nitrite/nitrate levels, aortic and brain oxidative stress levels ( aortic superoxide anion levels, brain thiobarbituric acid reactive species and brain glutathione levels) and brain acetylcholinesterase activity were also tested. STZ treated animals performed poorly on MWM hence reflecting impairment of learning and memory behavior with a significant reduction in body weight, impairment of vascular endothelial function, and decrease in serum nitrite/nitrate levels, increase in serum glucose, aortic and brain oxidative stress levels and brain acetylcholinesterase activity. Treatment of PPAR-γ agonists, pioglitazone as well as rosiglitazone significantly reversed, diabetes induced impairment of learning and memory behavior, endothelial function, and changes in various biochemical parameters. It is concluded that PPAR-γ modulators pioglitazone and rosiglitazone may be considered as potential pharmacological agents for the management of diabetes induced VaD. ► Streptozotocin (STZ) diabetes induces endothelial dysfunction & vascular dementia. ► Diabetes increases serum glucose, oxidative stress, AChE activity & decrease NO. ► PPAR-γ agonists attenuated diabetic endothelial dysfunction & vascular dementia. ► PPAR-γ agonists attenuated diabetes induced impairment of biochemical levels. ► PPAR-γ agonists have shown good benefit in STZ diabetes induced vascular dementia.
    Keywords: Vascular Endothelial Dysfunction ; Alzheimer'S Disease ; Pioglitazone ; Donepezil ; Morris Water Maze ; Oxidative Stress ; Pharmacy, Therapeutics, & Pharmacology ; Psychology
    ISSN: 0091-3057
    E-ISSN: 1873-5177
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