PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19604516-7 2009 These results indicate that JNK signaling pathway may be the major upstream mediator of regulation of COX-2 expression induced by MPTP in vivo and inhibiting JNK activity may represent a new and effective strategy to PD. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 130-134 cytochrome c oxidase II, mitochondrial Mus musculus 102-107 19604516-0 2009 JNK inhibitor protects dopaminergic neurons by reducing COX-2 expression in the MPTP mouse model of subacute Parkinson"s disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 80-84 cytochrome c oxidase II, mitochondrial Mus musculus 56-61 19604516-4 2009 In the present study, we investigated the role of c-Jun [1] N-terminal kinase (JNK) in the process of COX-2 expression in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of subacute PD. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 126-170 cytochrome c oxidase II, mitochondrial Mus musculus 102-107 19604516-4 2009 In the present study, we investigated the role of c-Jun [1] N-terminal kinase (JNK) in the process of COX-2 expression in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of subacute PD. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 172-176 cytochrome c oxidase II, mitochondrial Mus musculus 102-107 19604516-5 2009 Our data showed that MPTP induced a transient JNK activation of dopaminergic neurons, upregulated COX-2 expression in dopaminergic neurons, and caused the loss of dopaminergic neurons. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 21-25 cytochrome c oxidase II, mitochondrial Mus musculus 98-103 14561922-5 2003 Inhibition of COX-2 protein expression decreased the lesion caused by MPTP and protected the dopaminergic neurons in substantia nigra pars compacta. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 70-74 cytochrome c oxidase II, mitochondrial Mus musculus 14-19 17715026-9 2007 In mice treated with JNK inhibitor, the number of TH-positive neurons and TH expression level in the SN was only decreased by 15% and 20% as compared with the control group (P<0.001) 7 days after the fifth injection of MPTP, COX-2-positive cell number and COX-2 expression level were obviously reduced as compared with the model group (P<0.001), and p-c-Jun was expressed mainly in the cytoplasm of the neurons whose expression level in SN were significantly decreased 6 h after the third injection of MPTP. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 219-223 cytochrome c oxidase II, mitochondrial Mus musculus 225-230 17715026-9 2007 In mice treated with JNK inhibitor, the number of TH-positive neurons and TH expression level in the SN was only decreased by 15% and 20% as compared with the control group (P<0.001) 7 days after the fifth injection of MPTP, COX-2-positive cell number and COX-2 expression level were obviously reduced as compared with the model group (P<0.001), and p-c-Jun was expressed mainly in the cytoplasm of the neurons whose expression level in SN were significantly decreased 6 h after the third injection of MPTP. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 219-223 cytochrome c oxidase II, mitochondrial Mus musculus 256-261 14704277-5 2004 Furthermore, we have identified cyclooxygenase (COX) 2 as a molecular target of JNK activation and demonstrated that COX-2 is indispensable for MPTP-induced dopaminergic cell death. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 144-148 cytochrome c oxidase II, mitochondrial Mus musculus 32-54 14704277-5 2004 Furthermore, we have identified cyclooxygenase (COX) 2 as a molecular target of JNK activation and demonstrated that COX-2 is indispensable for MPTP-induced dopaminergic cell death. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 144-148 cytochrome c oxidase II, mitochondrial Mus musculus 117-122 19861252-1 2009 OBJECTIVE: To investigate the effect of p38 mitogen-activated protein kinase (p38MAPK) on the expression of COX-2 and caspase-3 in the substania nigra (SN) of mice with MPTP-induced Parkinson disease (PD). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 169-173 cytochrome c oxidase II, mitochondrial Mus musculus 108-113 17715026-0 2007 [Effect of phosphorylated c-Jun expression on COX-2 expression in the substantia nigra of MPTP mouse model of subacute Parkinson disease]. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 90-94 cytochrome c oxidase II, mitochondrial Mus musculus 46-51 17715026-1 2007 OBJECTIVE: To investigate the effect of phophorylated c-Jun (p-c-Jun) expression on the expression of COX-2 in the substantia nigra (SN) of the MPTP mouse model of subacute Parkinson disease (PD) and explore the possible mechanism of the dopaminergic (DA) neuron death in PD. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 144-148 cytochrome c oxidase II, mitochondrial Mus musculus 102-107 16566823-3 2006 Induction of COX-2 is also found in an experimental model of PD produced by administration of 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 139-143 cytochrome c oxidase II, mitochondrial Mus musculus 13-18 16566823-8 2006 COX-2 deficiency attenuated MPTP-induced microglial activation, degeneration of TH-positive cells, and loss of coordination. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 28-32 cytochrome c oxidase II, mitochondrial Mus musculus 0-5 16566823-9 2006 CONCLUSION: These results indicate that reducing COX-2 activity can mitigate the secondary and progressive loss of dopaminergic neurons as well as the motor deficits induced by MPTP, possibly by suppression of microglial activation in the SNpc. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 177-181 cytochrome c oxidase II, mitochondrial Mus musculus 49-54 15306248-3 2004 In this study, we present the expression of COX-1 and COX-2 mRNA and protein in striatum following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration to mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 99-143 cytochrome c oxidase II, mitochondrial Mus musculus 54-59 15306248-3 2004 In this study, we present the expression of COX-1 and COX-2 mRNA and protein in striatum following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration to mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 145-149 cytochrome c oxidase II, mitochondrial Mus musculus 54-59 15306248-13 2004 However, COX-2 mRNA and protein expressions increase after MPTP injury; the role of these findings remains obscure. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 59-63 cytochrome c oxidase II, mitochondrial Mus musculus 9-14 12183047-3 2002 MPTP (20 mg/kg, subcutaneously) was injected daily into COX-1- and COX-2-deficient mice and wild-type (WT) controls for five consecutive days. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 0-4 cytochrome c oxidase II, mitochondrial Mus musculus 67-72 12183047-7 2002 These results indicate that loss of COX-2 activity reduces MPTP-induced damage to the dopaminergic neurons of the SNc, but does not alter the levels of dopamine and its metabolites in the striatum. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 59-63 cytochrome c oxidase II, mitochondrial Mus musculus 36-41 12183047-8 2002 Interestingly, MPTP caused the same degree of loss of dopaminergic neurons in both COX-2(+/-) and COX-2(-/-) mice (20% loss). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 15-19 cytochrome c oxidase II, mitochondrial Mus musculus 83-88 12183047-8 2002 Interestingly, MPTP caused the same degree of loss of dopaminergic neurons in both COX-2(+/-) and COX-2(-/-) mice (20% loss). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 15-19 cytochrome c oxidase II, mitochondrial Mus musculus 98-103 12183047-9 2002 The results of this study indicate an important role of COX-2 in MPTP-induced neuronal degeneration and suggest the possibility that manipulation of the COX-2 could be an important target for therapeutic interventions in PD. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 65-69 cytochrome c oxidase II, mitochondrial Mus musculus 56-61 12183047-9 2002 The results of this study indicate an important role of COX-2 in MPTP-induced neuronal degeneration and suggest the possibility that manipulation of the COX-2 could be an important target for therapeutic interventions in PD. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 65-69 cytochrome c oxidase II, mitochondrial Mus musculus 153-158 23703110-5 2013 Using fish oil (0.0368 g EPA and 0.0184 g DHA, per day), melatonin (10 mg/kg/day), and vitamin E (50 mg/Kg/day) we have now shown that COX-2 activity, LPO and nitrite/nitrate levels were significantly increased in MPTP treated mice (p < 0.001) while fish oil, melatonin and vitamin E treatment were capable of decreasing significantly the outcome of all above noted parameters (p < 0.05). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 214-218 cytochrome c oxidase II, mitochondrial Mus musculus 135-140 11180504-0 2001 Inhibition of the cyclooxygenase isoenzymes COX-1 and COX-2 provide neuroprotection in the MPTP-mouse model of Parkinson"s disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 91-95 cytochrome c oxidase II, mitochondrial Mus musculus 54-59 11180504-1 2001 To study the possible role of the isoenzymes of cyclooxygenase COX-1 and COX-2 in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson"s disease we used acetylsalicylic acid, a COX-1/COX-2 inhibitor, in comparison with meloxicam, a preferential COX-2 inhibitor. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 86-90 cytochrome c oxidase II, mitochondrial Mus musculus 73-78 11180504-1 2001 To study the possible role of the isoenzymes of cyclooxygenase COX-1 and COX-2 in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson"s disease we used acetylsalicylic acid, a COX-1/COX-2 inhibitor, in comparison with meloxicam, a preferential COX-2 inhibitor. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 86-90 cytochrome c oxidase II, mitochondrial Mus musculus 211-216 11180504-1 2001 To study the possible role of the isoenzymes of cyclooxygenase COX-1 and COX-2 in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson"s disease we used acetylsalicylic acid, a COX-1/COX-2 inhibitor, in comparison with meloxicam, a preferential COX-2 inhibitor. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 86-90 cytochrome c oxidase II, mitochondrial Mus musculus 211-216 11180504-12 2001 In conclusion, the inhibition of either COX-1/COX-2 by acetylsalicylic acid or preferentially COX-2 by meloxicam provided a clear neuroprotection against MPTP-toxicity on the striatal and nigral levels. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 154-158 cytochrome c oxidase II, mitochondrial Mus musculus 94-99 31251998-6 2019 Moreover gliotic specific inflammatory markers like glial fibrillary acidic protein (GFAP), ionized calcium-binding adaptor protein-1 (Iba-1), iNOS and COX-2 were found to be expressed more in MPTP intoxicated mice, Further the levels of proinflammatory cytokines like IL-beta, IL-6, and TNF-alpha were significantly upregulated in MPTP intoxicated mice, these deleterious responses were diminished to extend neuroprotection by PHL treatment. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 193-197 cytochrome c oxidase II, mitochondrial Mus musculus 152-157 34587406-13 2021 Histopathological abnormalities and increased iNOS and COX-2 expression were noted in MPTP-induced mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 86-90 cytochrome c oxidase II, mitochondrial Mus musculus 55-60 26108182-6 2015 Inflammatory markers Cox-2, caspase-1, and NOS-2 were significantly upregulated in MPTP mouse spinal cord as compared to control. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 83-87 cytochrome c oxidase II, mitochondrial Mus musculus 21-26 21970803-6 2011 MPTP treatment up-regulated mRNA expression of inducible nitric oxide synthase (iNOS), neuronal NOS, cyclooxygenase (COX)-2, glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1, and increased production of nitric oxide (NO) and prostaglandin E2 (PGE2) (P < 0.05). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 0-4 cytochrome c oxidase II, mitochondrial Mus musculus 101-123 21291942-0 2011 Targeting oxidative stress, mitochondrial dysfunction and neuroinflammatory signaling by selective cyclooxygenase (COX)-2 inhibitors mitigates MPTP-induced neurotoxicity in mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 143-147 cytochrome c oxidase II, mitochondrial Mus musculus 99-121 21291942-2 2011 The present study was focused on the possible neuroprotective effect of selective cyclooxygenase (COX)-2-inhibitors: valdecoxib and NS-398 in 1-methyl-4-phenyl-1,2,3,6-tertahydropyridine (MPTP)-induced neurotoxicity in mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 188-192 cytochrome c oxidase II, mitochondrial Mus musculus 82-104 21291942-9 2011 The findings of the present study substantiate the neuroprotective role of selective COX-2 inhibitors in ameliorating MPTP-induced neurodegeneration in mice and suggest the possible therapeutic potential of these drugs in the management of PD. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 118-122 cytochrome c oxidase II, mitochondrial Mus musculus 85-90 21376018-10 2011 The number of dopaminergic neurons in the SNpc was significantly reduced by MPTP treatment, while the MPTP-induced neuronal loss was minimal upon treatment with propofol or the selective COX-2 inhibitor, NS-398. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 102-106 cytochrome c oxidase II, mitochondrial Mus musculus 187-192