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  1. Article ; Online: Discovery of (

    Luo, Guanglin / Chen, Ling / Kostich, Walter A / Hamman, Brian / Allen, Jason / Easton, Amy / Bourin, Clotilde / Gulianello, Michael / Lippy, Jonathan / Nara, Susheel / Maishal, Tarun Kumar / Thiyagarajan, Kamalraj / Jalagam, Prasadrao / Pattipati, Sreenivasulu Naidu / Dandapani, Kumaran / Dokania, Manoj / Vattikundala, Pradeep / Sharma, Vivek / Elavazhagan, Saravanan /
    Verma, Manoj Kumar / Das, Manish Lal / Wagh, Santosh / Balakrishnan, Anand / Johnson, Benjamin M / Santone, Kenneth S / Thalody, George / Denton, Rex / Saminathan, Hariharan / Holenarsipur, Vinay K / Kumar, Anoop / Rao, Abhijith / Putlur, Siva Prasad / Sarvasiddhi, Sarat Kumar / Shankar, Ganesh / Louis, Justin V / Ramarao, Manjunath / Conway, Charles M / Li, Yu-Wen / Pieschl, Rick / Tian, Yuan / Hong, Yang / Ditta, Jonathan / Mathur, Arvind / Li, Jianqing / Smith, Daniel / Pawluczyk, Joseph / Sun, Dawn / Yip, Shiuhang / Wu, Dauh-Rurng / Vetrichelvan, Muthalagu / Gupta, Anuradha / Wilson, Alan / Gopinathan, Suma / Wason, Suman / Bristow, Linda / Albright, Charles F / Bronson, Joanne J / Macor, John E / Dzierba, Carolyn D

    Journal of medicinal chemistry

    2022  Volume 65, Issue 6, Page(s) 4457–4480

    Abstract: Recent mouse knockout studies identified adapter protein-2 associated kinase 1 (AAK1) as a viable target for treating neuropathic pain. Potent small-molecule inhibitors of AAK1 have been identified and show efficacy in various rodent pain models. ( ...

    Abstract Recent mouse knockout studies identified adapter protein-2 associated kinase 1 (AAK1) as a viable target for treating neuropathic pain. Potent small-molecule inhibitors of AAK1 have been identified and show efficacy in various rodent pain models. (
    MeSH term(s) Amines ; Animals ; Brain ; Mice ; Neuralgia/drug therapy ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Rats ; Spinal Cord
    Chemical Substances Amines ; Protein Kinase Inhibitors
    Language English
    Publishing date 2022-03-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 218133-2
    ISSN 1520-4804 ; 0022-2623
    ISSN (online) 1520-4804
    ISSN 0022-2623
    DOI 10.1021/acs.jmedchem.1c02131
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Discovery and Optimization of Biaryl Alkyl Ethers as a Novel Class of Highly Selective, CNS-Penetrable, and Orally Active Adaptor Protein-2-Associated Kinase 1 (AAK1) Inhibitors for the Potential Treatment of Neuropathic Pain.

    Luo, Guanglin / Chen, Ling / Kostich, Walter A / Hamman, Brian / Allen, Jason / Easton, Amy / Bourin, Clotilde / Gulianello, Michael / Lippy, Jonathan / Nara, Susheel / Pattipati, Sreenivasulu Naidu / Dandapani, Kumaran / Dokania, Manoj / Vattikundala, Pradeep / Sharma, Vivek / Elavazhagan, Saravanan / Verma, Manoj Kumar / Lal Das, Manish / Wagh, Santosh /
    Balakrishnan, Anand / Johnson, Benjamin M / Santone, Kenneth S / Thalody, George / Denton, Rex / Saminathan, Hariharan / Holenarsipur, Vinay K / Kumar, Anoop / Rao, Abhijith / Putlur, Siva Prasad / Sarvasiddhi, Sarat Kumar / Shankar, Ganesh / Louis, Justin V / Ramarao, Manjunath / Conway, Charles M / Li, Yu-Wen / Pieschl, Rick / Tian, Yuan / Hong, Yang / Bristow, Linda / Albright, Charles F / Bronson, Joanne J / Macor, John E / Dzierba, Carolyn D

    Journal of medicinal chemistry

    2022  Volume 65, Issue 6, Page(s) 4534–4564

    Abstract: Recent mouse knockout studies identified adapter protein-2-associated kinase 1 (AAK1) as a viable target for treating neuropathic pain. BMS-986176/LX-9211 ( ...

    Abstract Recent mouse knockout studies identified adapter protein-2-associated kinase 1 (AAK1) as a viable target for treating neuropathic pain. BMS-986176/LX-9211 (
    MeSH term(s) Anesthetics, General ; Animals ; Ethers/therapeutic use ; Mice ; Neuralgia/drug therapy ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Rats ; Spinal Cord ; Structure-Activity Relationship
    Chemical Substances Anesthetics, General ; Ethers ; Protein Kinase Inhibitors
    Language English
    Publishing date 2022-03-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 218133-2
    ISSN 1520-4804 ; 0022-2623
    ISSN (online) 1520-4804
    ISSN 0022-2623
    DOI 10.1021/acs.jmedchem.1c02132
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Pathophysiology and drug therapy of tardive dyskinesia: current concepts and future perspectives.

    Kulkarni, Shrinivas K / Naidu, Pattipati S

    Drugs of today (Barcelona, Spain : 1998)

    2003  Volume 39, Issue 1, Page(s) 19–49

    Abstract: Nearly 1% of the world population suffers from schizophrenia, and neuroleptics are the major class of drugs used to treat this disorder. Neuroleptics are associated with wide variety of extrapyramidal side effects, such as akathesia, dystonia, ... ...

    Abstract Nearly 1% of the world population suffers from schizophrenia, and neuroleptics are the major class of drugs used to treat this disorder. Neuroleptics are associated with wide variety of extrapyramidal side effects, such as akathesia, dystonia, neuroleptic malignant syndrome, Parkinson-ism and tardive dyskinesia. Despite the awareness that neuroleptics could cause extrapyramidal side effects, these drugs remain the most effective means of treating schizophrenia and Tourette's syndrome, as well as for the management of behavioral disorders in developmentally disabled individuals. Tardive dyskinesia is a complex hyperkinetic syndrome consisting of choriform, athetoid or rhythmically abnormal involuntary movements. Estimates of the prevalence rate of tardive dyskinesia in patients receiving neuroleptics range from 0.5-70%, with an average prevalence rate of 24%. Despite much research, the pathogenesis of tardive dyskinesia remains elusive. So far, various neurochemical hypotheses have been proposed for the development of tardive dyskinesia. These include dopaminergic hypersensitivity, disturbed balance between dopamine and cholinergic systems, dysfunctions of striatonigral GABAergic neurons and excitotoxicity. Similarly, different suppressive agents have been tried with limited success. Recently, the role of oxidative stress and structural abnormality in the pathophysiology of tardive dyskinesia has gained much impetus. Induction of free radicals by neuroleptic drugs leading to the oxidative stress and resultant structural abnormality could be the key factor in the pathogenesis of tardive dyskinesia. This hypothesis has been supported by numerous reports that chronic neuroleptic treatment increases free radical production and causes structural damage. More recently, the genetic vulnerability for the predisposition for the development of tardive dyskinesia, i.e., pharmacogenetic aspect of tardive dyskinesia, is also gaining impetus as a research area, and is discussed in detail in this article.
    MeSH term(s) Animals ; Antipsychotic Agents/adverse effects ; Antipsychotic Agents/therapeutic use ; Clinical Trials as Topic/statistics & numerical data ; Dyskinesia, Drug-Induced/drug therapy ; Dyskinesia, Drug-Induced/metabolism ; Dyskinesia, Drug-Induced/physiopathology ; Humans ; Schizophrenia/drug therapy ; Schizophrenia/genetics ; Schizophrenia/metabolism
    Chemical Substances Antipsychotic Agents
    Language English
    Publishing date 2003-04-01
    Publishing country Spain
    Document type Journal Article ; Review
    ISSN 1699-3993
    ISSN 1699-3993
    DOI 10.1358/dot.2003.39.1.799430
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Differential effects of cyclooxygenase inhibitors on haloperidol-induced catalepsy.

    Naidu, Pattipati S / Kulkarni, Shrinivas K

    Progress in neuro-psychopharmacology & biological psychiatry

    2002  Volume 26, Issue 5, Page(s) 819–822

    Abstract: Prostaglandins (PGs) might play a role as putative transmitters or as modulators in the central nervous system (CNS). In the present study, haloperidol (1 mg/kg i.p.)-treated mice showed significant cataleptic behaviour. Naproxen, a nonselective ... ...

    Abstract Prostaglandins (PGs) might play a role as putative transmitters or as modulators in the central nervous system (CNS). In the present study, haloperidol (1 mg/kg i.p.)-treated mice showed significant cataleptic behaviour. Naproxen, a nonselective cyclooxygenase (COX) inhibitor, dose-dependently (5 and 10 mg/kg) antagonized the haloperidol-induced catalepsy in mice. Nimesulide, a preferential COX inhibitor, also dose-dependently reduced the cataleptic score in haloperidol treated animals at the first and second hour but not at the third and fourth hour of haloperidol treatment. Rofecoxib, a selective COX-2 inhibitor, did not show any effect on haloperidol-induced catalepsy. The major findings of the present study suggest that PGs might play a significant role in haloperidol-induced catalepsy. The findings of the present study further suggested that COX-1 derived rather than COX-2 derived PGs might play a potential role in haloperidol-induced catalepsy. In conclusions COX inhibitors can be screened as potential drug candidates for the treatment of neuroleptic-induced extrapyramidal side effects (EPS).
    MeSH term(s) Animals ; Catalepsy/chemically induced ; Catalepsy/drug therapy ; Catalepsy/enzymology ; Cyclooxygenase 1 ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/pharmacology ; Cyclooxygenase Inhibitors/therapeutic use ; Dose-Response Relationship, Drug ; Haloperidol/toxicity ; Isoenzymes/antagonists & inhibitors ; Isoenzymes/metabolism ; Male ; Membrane Proteins ; Mice ; Prostaglandin-Endoperoxide Synthases/metabolism
    Chemical Substances Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors ; Isoenzymes ; Membrane Proteins ; Cyclooxygenase 1 (EC 1.14.99.1) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1) ; Ptgs1 protein, mouse (EC 1.14.99.1) ; Haloperidol (J6292F8L3D)
    Language English
    Publishing date 2002-06
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 781181-0
    ISSN 1878-4216 ; 0278-5846
    ISSN (online) 1878-4216
    ISSN 0278-5846
    DOI 10.1016/s0278-5846(01)00289-5
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  5. Article ; Online: Inhibitory properties of ibuprofen and its amide analogues towards the hydrolysis and cyclooxygenation of the endocannabinoid anandamide.

    Fowler, Christopher J / Björklund, Emmelie / Lichtman, Aron H / Naidu, Pattipati S / Congiu, Cenzo / Onnis, Valentina

    Journal of enzyme inhibition and medicinal chemistry

    2012  Volume 28, Issue 1, Page(s) 172–182

    Abstract: A dual-action cyclooxygenase (COX)-fatty acid amide hydrolase (FAAH) inhibitor may have therapeutic usefulness as an analgesic, but a key issue is finding the right balance of inhibitory effects. This can be done by the design of compounds exhibiting ... ...

    Abstract A dual-action cyclooxygenase (COX)-fatty acid amide hydrolase (FAAH) inhibitor may have therapeutic usefulness as an analgesic, but a key issue is finding the right balance of inhibitory effects. This can be done by the design of compounds exhibiting different FAAH/COX-inhibitory potencies. In the present study, eight ibuprofen analogues were investigated. Ibuprofen (1), 2-(4-Isobutylphenyl)-N-(2-(3-methylpyridin-2-ylamino)-2-oxoethyl)propanamide (9) and N-(3-methylpyridin-2-yl)-2-(4'-isobutylphenyl)propionamide (2) inhibited FAAH with IC(50) values of 134, 3.6 and 0.52 µM respectively. The corresponding values for COX-1 were ~29, ~50 and ~60 µM, respectively. Using arachidonic acid as substrate, the compounds were weak inhibitors of COX-2. However, when anandamide was used as COX-2 substrate, potency increased, with approximate IC(50) values of ~6, ~10 and ~19 µM, respectively. Compound 2 was confirmed to be active in vivo in a murine model of visceral nociception, but the effects of the compound were not blocked by CB receptor antagonists.
    MeSH term(s) Amidohydrolases/antagonists & inhibitors ; Animals ; Arachidonic Acids/metabolism ; Chemistry Techniques, Synthetic ; Cyclooxygenase 1/metabolism ; Cyclooxygenase 2/metabolism ; Cyclooxygenase 2 Inhibitors/pharmacology ; Cyclooxygenase Inhibitors/chemistry ; Cyclooxygenase Inhibitors/pharmacology ; Disease Models, Animal ; Drug Design ; Endocannabinoids/metabolism ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/pharmacology ; Hydrolysis ; Ibuprofen/analogs & derivatives ; Ibuprofen/pharmacology ; Inhibitory Concentration 50 ; Male ; Mice ; Mice, Inbred C57BL ; Polyunsaturated Alkamides/metabolism ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Visceral Pain/drug therapy
    Chemical Substances Arachidonic Acids ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors ; Endocannabinoids ; Enzyme Inhibitors ; Polyunsaturated Alkamides ; Cyclooxygenase 1 (EC 1.14.99.1) ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS1 protein, human (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; Amidohydrolases (EC 3.5.-) ; fatty-acid amide hydrolase (EC 3.5.1.-) ; anandamide (UR5G69TJKH) ; Ibuprofen (WK2XYI10QM)
    Language English
    Publishing date 2012-01-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2082578-X
    ISSN 1475-6374 ; 1475-6366
    ISSN (online) 1475-6374
    ISSN 1475-6366
    DOI 10.3109/14756366.2011.643304
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  6. Article: Neuroprotective effect of nimesulide, a preferential COX-2 inhibitor, against pentylenetetrazol (PTZ)-induced chemical kindling and associated biochemical parameters in mice.

    Dhir, Ashish / Naidu, Pattipati S / Kulkarni, Shrinivas K

    Seizure

    2007  Volume 16, Issue 8, Page(s) 691–697

    Abstract: Brain cyclooxygenases (COX), the rate-limiting enzyme in prostaglandin synthesis, is rapidly and transiently induced by convulsions in hippocampal and cortical neurons. Previous studies have explored the protective effect of naproxen (non-selective COX- ... ...

    Abstract Brain cyclooxygenases (COX), the rate-limiting enzyme in prostaglandin synthesis, is rapidly and transiently induced by convulsions in hippocampal and cortical neurons. Previous studies have explored the protective effect of naproxen (non-selective COX-inhibitor) or rofecoxib (selective COX-2 inhibitor) against chemical kindling in mice. With this background, the present study was designed to explore the possible effect of nimesulide (a preferential COX-2 inhibitor) against pentylenetetrazol (PTZ)-induced kindling epilepsy in mice. To induce kindling, PTZ was injected in a subconvulsive dose (40 mg/kg, i.p.) every other day for 15 days. Nimesulide (2.5 or 5 mg/kg, p.o.) was administered each day 45 min before either PTZ or vehicle challenge. The intensity of kindling was assessed immediately after PTZ administration according to a prevalidated scoring scale. On 16th day i.e. 24 h after the last dose of PTZ, animals were sacrificed and various biochemical parameters were assessed in the whole brain. Compared with normal control group, PTZ-kindled mice had significantly higher levels of malondialdehyde, nitrite, myeloperoxidase but had lower levels of reduced glutathione in the whole brain homogenate. Chronic treatment with nimesulide (2.5 or 5 mg/kg, p.o.) for 15 days showed significant decrease in kindling score and could play a role in controlling the accompanying biochemical alterations due to PTZ. These results suggested that nimesulide, a preferential COX-2 inhibitor offered neuroprotection against PTZ-induced kindling in mice.
    MeSH term(s) Analysis of Variance ; Animals ; Behavior, Animal ; Brain Chemistry/drug effects ; Cyclooxygenase Inhibitors/administration & dosage ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Drug Interactions ; Epilepsy/chemically induced ; Epilepsy/drug therapy ; Glutathione/metabolism ; Kindling, Neurologic/drug effects ; Lipid Peroxidation/drug effects ; Male ; Mice ; Nitrites/metabolism ; Pentylenetetrazole ; Peroxidase/metabolism ; Sulfonamides/administration & dosage ; Time Factors
    Chemical Substances Cyclooxygenase Inhibitors ; Nitrites ; Sulfonamides ; Peroxidase (EC 1.11.1.7) ; Glutathione (GAN16C9B8O) ; nimesulide (V4TKW1454M) ; Pentylenetetrazole (WM5Z385K7T)
    Language English
    Publishing date 2007-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 1137610-7
    ISSN 1532-2688 ; 1059-1311
    ISSN (online) 1532-2688
    ISSN 1059-1311
    DOI 10.1016/j.seizure.2007.05.016
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    Zs.A 3573: Show issues Location:
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  7. Article: Effect of cyclooxygenase inhibitors on pentylenetetrazol (PTZ)-induced convulsions: Possible mechanism of action.

    Dhir, Ashish / Naidu, Pattipati S / Kulkarni, Shrinivas K

    Progress in neuro-psychopharmacology & biological psychiatry

    2006  Volume 30, Issue 8, Page(s) 1478–1485

    Abstract: Cyclooxygenase (COX) is reported to play a significant role in neurodegenerative and neuropsychiatric disorders, and may play a significant role in the pathogenesis of epilepsy. Various neurotransmitter abnormalities, especially of GABA and glutamate, ... ...

    Abstract Cyclooxygenase (COX) is reported to play a significant role in neurodegenerative and neuropsychiatric disorders, and may play a significant role in the pathogenesis of epilepsy. Various neurotransmitter abnormalities, especially of GABA and glutamate, have been reported to play a key role in the pathophysiology of epilepsy. The objective of the present study was to elucidate the effect of cyclooxygenase inhibitors on pentylenetetrazol (PTZ)-induced (80 mg/kg) convulsions in mice with possible mechanism of action. Various COX-inhibitors were administered 45 min prior to the PTZ administration. Onset, duration of clonic convulsions and percentage mortality/recovery were recorded. Pretreatment with COX-inhibitors aspirin (10 and 20 mg/kg, p.o.), naproxen (7 and 14 mg/kg, p.o.), nimesulide (1-5 mg/kg, p.o.) or rofecoxib (1-4 mg/kg, p.o.) dose-dependently showed protection against PTZ-induced convulsions. COX-2 inhibitors were more effective as compared to non-selective COX-inhibitors. Rofecoxib (1 mg/kg) or nimesulide (1 mg/kg) also enhanced the sub-protective effect of diazepam or muscimol showing GABAergic modulation of COX-2 inhibitors. COX-2 inhibitors also antagonized the effect of flumazenil (4 mg/kg)- against PTZ-induced convulsions further confirming the GABAergic mechanism. In conclusion, the results of the present study strongly suggest the possible role of cyclooxygenase isoenzymes in the pathophysiology of epilepsy and the use of COX-inhibitors as an adjuvant therapy in the treatment of epilepsy.
    MeSH term(s) Animals ; Anticonvulsants/therapeutic use ; Convulsants/pharmacology ; Cyclooxygenase Inhibitors/therapeutic use ; Diazepam/pharmacology ; Disease Models, Animal ; Male ; Mice ; Pentylenetetrazole/pharmacology ; Seizures/chemically induced ; Seizures/prevention & control
    Chemical Substances Anticonvulsants ; Convulsants ; Cyclooxygenase Inhibitors ; Diazepam (Q3JTX2Q7TU) ; Pentylenetetrazole (WM5Z385K7T)
    Language English
    Publishing date 2006-12-30
    Publishing country England
    Document type Journal Article
    ZDB-ID 781181-0
    ISSN 1878-4216 ; 0278-5846
    ISSN (online) 1878-4216
    ISSN 0278-5846
    DOI 10.1016/j.pnpbp.2006.06.003
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  8. Article: Effect of cyclooxygenase-2 (COX-2) inhibitors in various animal models (bicuculline, picrotoxin, maximal electroshock-induced convulsions) of epilepsy with possible mechanism of action.

    Dhir, Ashish / Naidu, Pattipati S / Kulkarni, Shrinivas K

    Indian journal of experimental biology

    2006  Volume 44, Issue 4, Page(s) 286–291

    Abstract: Enzyme cyclooxygenase (COX) is reported to play a significant role in neurodegeneration and may play a significant role in the pathogenesis of epilepsy. Bicuculline (4 mg/kg; ip), picrotoxin (8 mg/kg; ip) and electroshock (60 mA for 0.2 sec) ... ...

    Abstract Enzyme cyclooxygenase (COX) is reported to play a significant role in neurodegeneration and may play a significant role in the pathogenesis of epilepsy. Bicuculline (4 mg/kg; ip), picrotoxin (8 mg/kg; ip) and electroshock (60 mA for 0.2 sec) significantly induced convulsions in male Laka mice. COX-inhibitors viz. nimesulide (2.5 mg/kg; ip) and rofecoxib (2 mg/kg, ip) administered 45 minutes prior to an epileptic challenge prolonged mean onset time of convulsions, decreased duration of clonus and decreased % mortality rate against bicuculline- and picrotoxin-induced convulsions in mice. COX-2 inhibitors were ineffective towards maximal electroshock-induced convulsions. Nimesulide (1 mg/kg) and rofecoxib (1 mg/kg) also enhanced the effect of subprotective dose of muscimol against picrotoxin-induced convulsions. The result of the present study strongly suggests for a possible role of cyclooxygenase isoenzymes particularly, COX-2 in the pathophysiology of epilepsy and its GABAergic modulation.
    MeSH term(s) Animals ; Bicuculline/pharmacology ; Cyclooxygenase 2/metabolism ; Cyclooxygenase Inhibitors/pharmacology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Electroshock/adverse effects ; Male ; Mice ; Muscimol/pharmacology ; Picrotoxin/pharmacology ; Seizures/chemically induced ; Seizures/enzymology
    Chemical Substances Cyclooxygenase Inhibitors ; Picrotoxin (124-87-8) ; Muscimol (2763-96-4) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Bicuculline (Y37615DVKC)
    Language English
    Publishing date 2006-04
    Publishing country India
    Document type Journal Article
    ZDB-ID 416061-7
    ISSN 0975-1009 ; 0019-5189
    ISSN (online) 0975-1009
    ISSN 0019-5189
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Effect of Withania somnifera root extract on reserpine-induced orofacial dyskinesia and cognitive dysfunction.

    Naidu, Pattipati S / Singh, Amanpreet / Kulkarni, Shrinivas K

    Phytotherapy research : PTR

    2006  Volume 20, Issue 2, Page(s) 140–146

    Abstract: Tardive dyskinesia is one of the major side effects of long-term neuroleptic treatment. The pathophysiology of this disabling and commonly irreversible movement disorder is still obscure. Vacuous chewing movements in rats are widely accepted as an animal ...

    Abstract Tardive dyskinesia is one of the major side effects of long-term neuroleptic treatment. The pathophysiology of this disabling and commonly irreversible movement disorder is still obscure. Vacuous chewing movements in rats are widely accepted as an animal model of tardive dyskinesia. Oxidative stress and products of lipid peroxidation are implicated in the pathophysiology of tardive dyskinesia. Repeated treatment with reserpine (1.0 mg/kg) on alternate days for a period of 5 days (days 1, 3 and 5) significantly induced vacuous chewing movements and tongue protrusions in rats. Chronic treatment with Withania somnifera root extract (Ws) for a period of 4 weeks to reserpine treated animals significantly and dose dependently (50 and 100 mg/kg) reduced the reserpine-induced vacuous chewing movements and tongue protrusions. Reserpine treated animals also showed poor retention of memory in the elevated plus maze task paradigm. Chronic Ws administration significantly reversed reserpine-induced retention deficits. Biochemical analysis revealed that chronic reserpine treatment significantly induced lipid peroxidation and decreased the glutathione (GSH) levels in the brains of rats. Chronic reserpine treated rats showed decreased levels of antioxidant defense enzymes, superoxide dismutase (SOD) and catalase. Chronic administration of Ws root extract dose dependently (50 and 100 mg/kg) and significantly reduced the lipid peroxidation and restored the decreased glutathione levels by chronic reserpine treatment. It also significantly reversed the reserpine-induced decrease in brain SOD and catalase levels in rats. The major findings of the present study indicate that oxidative stress might play an important role in the pathophysiology of reserpine-induced abnormal oral movements. In conclusion, Withania somnifera root extract could be a useful drug for the treatment of drug-induced dyskinesia.
    MeSH term(s) Animals ; Antioxidants/metabolism ; Brain/enzymology ; Brain/metabolism ; Cognition Disorders/chemically induced ; Cognition Disorders/complications ; Cognition Disorders/drug therapy ; Cognition Disorders/metabolism ; Dyskinesia, Drug-Induced/complications ; Dyskinesia, Drug-Induced/drug therapy ; Dyskinesia, Drug-Induced/metabolism ; Glutathione/metabolism ; Male ; Malondialdehyde/metabolism ; Phytotherapy ; Plant Extracts/therapeutic use ; Plant Roots ; Rats ; Rats, Wistar ; Reserpine ; Withania
    Chemical Substances Antioxidants ; Plant Extracts ; Malondialdehyde (4Y8F71G49Q) ; Reserpine (8B1QWR724A) ; Glutathione (GAN16C9B8O)
    Language English
    Publishing date 2006-02
    Publishing country England
    Document type Journal Article
    ZDB-ID 639136-9
    ISSN 1099-1573 ; 0951-418X
    ISSN (online) 1099-1573
    ISSN 0951-418X
    DOI 10.1002/ptr.1823
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Effect of rofecoxib, a cyclo-oxygenase-2 inhibitor, on various biochemical parameters of brain associated with pentylenetetrazol-induced chemical kindling in mice.

    Dhir, Ashish / Naidu, Pattipati S / Kulkarni, Shrinivas K

    Fundamental & clinical pharmacology

    2006  Volume 20, Issue 3, Page(s) 255–261

    Abstract: Cyclo-oxygenase (COX) has been reported to play a significant role in neurodegeneration and other brain-related disorders. Recent studies have reported that COX plays a significant role in the pathophysiology of brain-related disorders and COX-2 ... ...

    Abstract Cyclo-oxygenase (COX) has been reported to play a significant role in neurodegeneration and other brain-related disorders. Recent studies have reported that COX plays a significant role in the pathophysiology of brain-related disorders and COX-2 inhibitors could be useful drug therapy in neurodegenerative disorders. The aim of the present study was to explore the possible role of COX and the effect of COX-2 inhibitor, rofecoxib in epilepsy. In the present study, kindling was induced in mice by chronic administration of a subconvulsive dose of pentylenetetrazol (PTZ, 40 mg/kg, i.p.) on every other day for a period of 15 days. Rofecoxib was administered orally daily 45 min before either PTZ or vehicle. The kindling score was recorded after PTZ administration. Seizure severity was measured according to a prevalidated scoring scale. Biochemical estimations were performed on the day 16 of PTZ treatment (24 h after the last dose of PTZ). Chronic treatment with selective COX-2 inhibitor, rofecoxib (2.0 and 5.0 mg/kg, p.o.) for 15 days showed significant decrease in PTZ-induced kindling score. Biochemical analysis showed that chronic treatment with PTZ significantly increased lipid peroxidation, nitrite levels (NO levels), and myeloperoxidase levels and decreased the reduced glutathione levels in brain homogenate. Chronic treatment with rofecoxib, a selective COX-2 inhibitor, significantly reversed the PTZ-induced kindling score as well as various biochemical alterations suggesting the use of COX-2 inhibitor rofecoxib in epilepsy. In conclusion, results of the present study suggested that COX-2 plays an important role in the pathophysiology of PTZ-induced kindling in mice and rofecoxib is protective against various biochemical alterations against PTZ-induced kindling in mice.
    MeSH term(s) Animals ; Brain/drug effects ; Brain/metabolism ; Cyclooxygenase 2 Inhibitors/pharmacology ; Dose-Response Relationship, Drug ; Glutathione/metabolism ; Kindling, Neurologic ; Lactones/pharmacology ; Male ; Malondialdehyde/metabolism ; Mice ; Nitrites/metabolism ; Pentylenetetrazole/administration & dosage ; Peroxidase/metabolism ; Sulfones/pharmacology ; Time Factors
    Chemical Substances Cyclooxygenase 2 Inhibitors ; Lactones ; Nitrites ; Sulfones ; rofecoxib (0QTW8Z7MCR) ; Malondialdehyde (4Y8F71G49Q) ; Peroxidase (EC 1.11.1.7) ; Glutathione (GAN16C9B8O) ; Pentylenetetrazole (WM5Z385K7T)
    Language English
    Publishing date 2006-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 639134-5
    ISSN 1472-8206 ; 0767-3981
    ISSN (online) 1472-8206
    ISSN 0767-3981
    DOI 10.1111/j.1472-8206.2006.00398.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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