Araştırma Makalesi
BibTex RIS Kaynak Göster
Yıl 2024, , 166 - 177, 31.05.2024
https://doi.org/10.5472/marumj.1480086

Öz

Kaynakça

  • von Campenhausen S, Bornschein B, Wick R et al. Prevalence and incidence of Parkinson’s disease in Europe. Eur Neuropsychopharmacol 2005; 15: 473-90. doi: 10.1016/j. euroneuro.2005.04.007.
  • Aarsland D, Batzu L, Halliday G M et al. Parkinson diseaseassociated cognitive impairment. Nat Rev Dis Primers 2021; 7: 47. doi: 10.1038/s41572.021.00280-3.
  • Dauer W and Przedborski S. Parkinson’s disease: mechanisms and models. Neuron 2003; 39: 889-909.
  • Exner N, Lutz A K, Haass C, Winklhofer K F. Mitochondrial dysfunction in Parkinson’s disease: molecular mechanisms and pathophysiological consequences. Embo J 2012; 31: 3038- 62. doi: 10.1038/emboj.2012.170.
  • Ebrahimi-Fakhari D, Wahlster L, and McLean P J. Protein degradation pathways in Parkinson’s disease: curse or blessin. Acta Neuropathol 2012; 124: 153-72. doi: 10.1007/ s00401.012.1004-6.
  • Stefanis L. α-Synuclein in Parkinson’s disease. Cold Spring Harb Perspect Med 2012; 2: a009399. doi: 10.1101/cshperspect. a009399.
  • Hetz C, Saxena S. ER stress and the unfolded protein response in neurodegeneration. Nat Rev Neurol 2017; 13: 477-91. doi: 10.1038/nrneurol.2017.99.
  • Ascherio A, Schwarzschild M A. The epidemiology of Parkinson’s disease: risk factors and prevention. Lancet Neurol 2016; 15: 1257-72. doi: 10.1016/s1474-4422(16)30230-7.
  • De Pablo-Fernandez E, Goldacre R, Pakpoor J, Noyce A J, Warner T T. Association between diabetes and subsequent Parkinson disease: A record-linkage cohort study. Neurology 2018; 91: e139-e142. doi: 10.1212/ wnl.000.000.0000005771.
  • Cereda E, Barichella M, Pedrolli C, et al. Diabetes and risk of Parkinson’s disease: a systematic review and meta-analysis. Diabetes Care 2011; 34: 2614-23. doi: 10.2337/dc11-1584.
  • Sandyk R. The relationship between diabetes mellitus and Parkinson’s disease Int J Neurosci 1993; 69: 125-30. doi: 10.3109/002.074.59309003322.
  • Galicia-Garcia U, Benito-Vicente A, Jebari S, et al. Pathophysiology of Type 2 diabetes mellitus. Int J Mol Sci 2020; 21:6275. doi: 10.3390/ijms21176275.
  • Henriksen E J, Diamond-Stanic M K, Marchionne E M. Oxidative stress and the etiology of insulin resistance and type 2 diabetes. Free Radic Biol Med 2011; 51: 993-9. doi: 10.1016/j. freeradbiomed.2010.12.005.
  • Nowotny K, Jung T, Höhn A, Weber D, Grune T. Advanced glycation end products and oxidative stress in type 2 diabetes mellitus. Biomolecules 2015; 5: 194-222. doi: 10.3390/ biom5010194.
  • Dornadula S, Elango B, Balashanmugam P, Palanisamy R, Kunka Mohanram R. Pathophysiological insights of methylglyoxal induced type-2 diabetes. Chem Res Toxicol 2015; 28: 1666-74. doi: 10.1021/acs.chemrestox.5b00171.
  • Lu J, Randell E, Han Y, Adeli K, Krahn J, Meng Q H. Increased plasma methylglyoxal level, inflammation, and vascular endothelial dysfunction in diabetic nephropathy. Clin Biochem 2011; 44: 307-11. doi: 10.1016/j. clinbiochem.2010.11.004.
  • Vicente Miranda H, Szego É M, Oliveira L M A, et al. Glycation potentiates α-synuclein-associated neurodegeneration in synucleinopathies. Brain 2017; 140: 1399-419. doi: 10.1093/ brain/awx056.
  • Biosa A, Outeiro T F, Bubacco L, Bisaglia M. Diabetes mellitus as a risk factor for Parkinson’s disease: a molecular point of view. Mol Neurobiol 2018; 55: 8754-63. doi: 10.1007/ s12035.018.1025-9.
  • Fitzmaurice A G, Rhodes S L, Lulla A, et al. Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease. Proc Natl Acad Sci U S A 2013; 110: 636- 41. doi: 10.1073/pnas.122.039.9110.
  • Zhang Z N, Zhang J S, Xiang J, et al. Subcutaneous rotenone rat model of Parkinson’s disease: Dose exploration study. Brain Res 2017; 1655: 104-13. doi: 10.1016/j.brainres.2016.11.020.
  • Meredith G E, Kang U J. Behavioral models of Parkinson’s disease in rodents: a new look at an old problem. Mov Disord 2006; 21: 1595-606. doi: 10.1002/mds.21010.
  • Fleming S M, Zhu C, Fernagut P O, et al. Behavioral and immunohistochemical effects of chronic intravenous and subcutaneous infusions of varying doses of rotenone. Exp Neurol 2004; 187: 418-29. doi: 10.1016/j. expneurol.2004.01.023.
  • Sharma M, Kaur J, Rakshe S, Sharma N, Khunt D, Khairnar A. Intranasal exposure to low-dose rotenone Induced alphasynuclein accumulation and Parkinson’s like symptoms without loss of dopaminergic neurons. Neurotox Res 2022; 40: 215-29. doi: 10.1007/s12640.021.00436-9.
  • Paxinos G, Watson C. The rat brain in stereotaxic coordinates. Hard cover 6th edition. Elsevier, 2006.
  • Bao L, Avshalumov M V, Rice M E. Partial mitochondrial inhibition causes striatal dopamine release suppression and medium spiny neuron depolarization via H2O2 elevation, not ATP depletion. J Neurosci 2005; 25: 10029-40. doi: 10.1523/ jneurosci.2652-05.2005.
  • Alam M, Danysz W, Schmidt W J, Dekundy A. Effects of glutamate and alpha2-noradrenergic receptor antagonists on the development of neurotoxicity produced by chronic rotenone in rats. Toxicol Appl Pharmacol 2009; 240: 198-207. doi: 10.1016/j.taap.2009.07.010.
  • Cenci M A, Francardo V, O’Sullivan S S, Lindgren H S. Rodent models of impulsive-compulsive behaviors in Parkinson’s disease: How far have we reached? Neurobiol Dis 2015; 82: 561-73. doi: 10.1016/j.nbd.2015.08.026.
  • Samii A, Nutt J G, Ransom B R. Parkinson’s disease. Lancet 2004; 363: 1783-93. doi: 10.1016/s0140-6736(04)16305-8.
  • Kravitz A V, Freeze B S, Parker P R, et al. Regulation of parkinsonian motor behaviours by optogenetic control of basal ganglia circuitry, Nature, 2010; 466: 622-6. doi: 10.1038/ nature09159.
  • Cataldi S, Stanley A T, Miniaci M C, Sulzer D. Interpreting the role of the striatum during multiple phases of motor learning. Febs j, 2022; 289: 2263-2281. doi: 10.1111/febs.15908.
  • Chegão A, Guarda M, Alexandre B M et al. Glycation modulates glutamatergic signaling and exacerbates Parkinson’s disease-like phenotypes, NPJ Parkinsons Dis 2022; 8: 51. doi: 10.1038/s41531.022.00314-x.
  • Panigrahi B, Martin K A, Li Y, et al. Dopamine is required for the neural representation and control of movement vigor. Cell, 2015; 162: 1418-30. doi: 10.1016/j.cell.2015.08.014.
  • Taylor T N, Greene J G, Miller G W. Behavioral phenotyping of mouse models of Parkinson’s disease. Behav Brain Res 2010; 211: 1-10. doi: 10.1016/j.bbr.2010.03.004.
  • Su R J, Zhen J L, Wang W, Zhang J L, Zheng Y, Wang X M. Timecourse behavioral features are correlated with Parkinson’s disease‑associated pathology in a 6-hydroxydopamine hemiparkinsonian rat model. Mol Med Rep 2018; 17: 3356-63. doi: 10.3892/mmr.2017.8277.
  • Lissner L J, Rodrigues L, Wartchow K M, et al. Shortterm alterations in behavior and astroglial function after intracerebroventricular infusion of methylglyoxal in rats. Neurochem Res 2021; 46: 183-96. doi: 10.1007/ s11064.020.03154-4.
  • Szczepanik J C, de Almeida G R L, Cunha M P, Dafre A L. Repeated methylglyoxal treatment depletes dopamine in the prefrontal cortex, and causes memory impairment and depressive-like behavior in mice, Neurochem Res 2020; 45: 354-70. doi: 10.1007/s11064.019.02921-2.
  • Hipkiss A R. On the relationship between energy metabolism, proteostasis, aging and Parkinson’s disease: Possible causative role of methylglyoxal and alleviative potential of carnosine. Aging Dis 2017; 8: 334-45. doi: 10.14336/ad.2016.1030.
  • Distler M G, Plant L D, Sokoloff G, et al. Glyoxalase 1 increases anxiety by reducing GABAA receptor agonist methylglyoxal. J Clin Invest 2012; 122: 2306-15. doi: 10.1172/jci61319.
  • Nehru B, Verma R, Khanna P, Sharma S K. Behavioral alterations in rotenone model of Parkinson’s disease: attenuation by co-treatment of centrophenoxine. Brain Res 2008; 1201: 122-7. doi: 10.1016/j.brainres.2008.01.074.
  • Palle S, Neerati P. Improved neuroprotective effect of resveratrol nanoparticles as evinced by abrogation of rotenoneinduced behavioral deficits and oxidative and mitochondrial dysfunctions in rat model of Parkinson’s disease. Naunyn Schmiedebergs Arch Pharmacol 2018; 391: 445-53. doi: 10.1007/s00210.018.1474-8.
  • Kandil E A, Abdelkader N F, El-Sayeh B M, Saleh S. Imipramine and amitriptyline ameliorate the rotenone model of Parkinson’s disease in rats. Neuroscience. 2016; 332: 26-37. doi: 10.1016/j.neuroscience.2016.06.040.
  • Greenamyre J T, Cannon J R, Drolet R, Mastroberardino P G. Lessons from the rotenone model of Parkinson’s disease. Trends Pharmacol Sci 2010; 31: 141-2; author reply 142-3. doi: 10.1016/j.tips.2009.12.006.
  • Khadrawy Y A, Salem A M, El-Shamy K A, Ahmed E K, Fadl N N, Hosny E N. Neuroprotective and therapeutic effect of caffeine on the rat model of Parkinson’s disease induced by rotenone. J Diet Suppl 2017; 14: 553-72. doi: 10.1080/19390.211.2016.1275916.
  • Greene J G, Noorian A R, Srinivasan S. Delayed gastric emptying and enteric nervous system dysfunction in the rotenone model of Parkinson’s disease. Exp Neurol 2009; 218: 154-61. doi: 10.1016/j.expneurol.2009.04.023.
  • Drolet R E, Cannon J R, Montero L, Greenamyre J T. Chronic rotenone exposure reproduces Parkinson’s disease gastrointestinal neuropathology. Neurobiol Dis 2009; 36: 96- 102. doi: 10.1016/j.nbd.2009.06.017.
  • Sharma N, Khurana N, Muthuraman A, Utreja P. Pharmacological evaluation of vanillic acid in rotenoneinduced Parkinson’s disease rat model. Eur J Pharmacol 2021; 903: 174112. doi: 10.1016/j.ejphar.2021.174112.
  • Ravenstijn P G, Merlini M, Hameetman M, et al. The exploration of rotenone as a toxin for inducing Parkinson’s disease in rats, for application in BBB transport and PK-PD experiments. J Pharmacol Toxicol Methods 2008; 57: 114-30. doi: 10.1016/j.vascn.2007.10.003.
  • Jia X, Olson D J, Ross A R, Wu L. Structural and functional changes in human insulin induced by methylglyoxal. Faseb J 2006; 20: 1555-7. doi: 10.1096/fj.05-5478fje.
  • Dhar A, Dhar I, Jiang B, Desai K M, Wu L. Chronic methylglyoxal infusion by minipump causes pancreatic betacell dysfunction and induces type 2 diabetes in Sprague- Dawley rats. Diabetes 2011; 60: 899-908. doi: 10.2337/db10- 0627.
  • Ankrah N A, Appiah-Opong R. Toxicity of low levels of methylglyoxal: depletion of blood glutathione and adverse effect on glucose tolerance in mice. Toxicol Lett 1999; 109: 61- 7. doi: 10.1016/s0378-4274(99)00114-9.
  • Matafome P, Santos-Silva D, Crisóstomo J, et al. Methylglyoxal causes structural and functional alterations in adipose tissue independently of obesity. Arch Physiol Biochem 2012; 118: 58-68. doi: 10.3109/13813.455.2012.658065.

Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model

Yıl 2024, , 166 - 177, 31.05.2024
https://doi.org/10.5472/marumj.1480086

Öz

Objective: Type 2 diabetes mellitus patients have been reported to have a higher incidence of Parkinson’s disease. This study aimed to
explore the effect of advanced glycation end products precursor methylglyoxal (MGO) on the pathophysiology of Parkinson’s disease
in a rotenone model.
Materials and Methods: Adult female Wistar rats (n=42) were divided into four groups. Rotenone toxicity was assessed by daily weight
measurements and mortality rates. Effect of MGO on blood glucose was evaluated. Locomotor activity, rearing, and rotarod tests
were performed to evaluate motor functions, and for neurodegeneration, tyrosine hydroxylase immunoreactivity in the striatum and
substantia nigra regions was assessed.
Results: The mortality rate was 9% in the rotenone-applied rats. The mean weight, locomotor activity, rearing activity, and longest time
spent on a rotarod were lower in the MGO+Rotenone group than in the Control group. Tyrosine hydroxylase immunoreactivity in the
striatum rostral to the anterior commissure in the MGO+Rotenone group was lower than that in the Control and MGO groups. The
number of tyrosine hydroxylase positive cells in the substantia nigra pars compacta was comparable among the groups.
Conclusion: When nigrostriatal degeneration was triggered, MGO was found to worsen motor dysfunction and increase damage to
dopaminergic neuron projections.

Kaynakça

  • von Campenhausen S, Bornschein B, Wick R et al. Prevalence and incidence of Parkinson’s disease in Europe. Eur Neuropsychopharmacol 2005; 15: 473-90. doi: 10.1016/j. euroneuro.2005.04.007.
  • Aarsland D, Batzu L, Halliday G M et al. Parkinson diseaseassociated cognitive impairment. Nat Rev Dis Primers 2021; 7: 47. doi: 10.1038/s41572.021.00280-3.
  • Dauer W and Przedborski S. Parkinson’s disease: mechanisms and models. Neuron 2003; 39: 889-909.
  • Exner N, Lutz A K, Haass C, Winklhofer K F. Mitochondrial dysfunction in Parkinson’s disease: molecular mechanisms and pathophysiological consequences. Embo J 2012; 31: 3038- 62. doi: 10.1038/emboj.2012.170.
  • Ebrahimi-Fakhari D, Wahlster L, and McLean P J. Protein degradation pathways in Parkinson’s disease: curse or blessin. Acta Neuropathol 2012; 124: 153-72. doi: 10.1007/ s00401.012.1004-6.
  • Stefanis L. α-Synuclein in Parkinson’s disease. Cold Spring Harb Perspect Med 2012; 2: a009399. doi: 10.1101/cshperspect. a009399.
  • Hetz C, Saxena S. ER stress and the unfolded protein response in neurodegeneration. Nat Rev Neurol 2017; 13: 477-91. doi: 10.1038/nrneurol.2017.99.
  • Ascherio A, Schwarzschild M A. The epidemiology of Parkinson’s disease: risk factors and prevention. Lancet Neurol 2016; 15: 1257-72. doi: 10.1016/s1474-4422(16)30230-7.
  • De Pablo-Fernandez E, Goldacre R, Pakpoor J, Noyce A J, Warner T T. Association between diabetes and subsequent Parkinson disease: A record-linkage cohort study. Neurology 2018; 91: e139-e142. doi: 10.1212/ wnl.000.000.0000005771.
  • Cereda E, Barichella M, Pedrolli C, et al. Diabetes and risk of Parkinson’s disease: a systematic review and meta-analysis. Diabetes Care 2011; 34: 2614-23. doi: 10.2337/dc11-1584.
  • Sandyk R. The relationship between diabetes mellitus and Parkinson’s disease Int J Neurosci 1993; 69: 125-30. doi: 10.3109/002.074.59309003322.
  • Galicia-Garcia U, Benito-Vicente A, Jebari S, et al. Pathophysiology of Type 2 diabetes mellitus. Int J Mol Sci 2020; 21:6275. doi: 10.3390/ijms21176275.
  • Henriksen E J, Diamond-Stanic M K, Marchionne E M. Oxidative stress and the etiology of insulin resistance and type 2 diabetes. Free Radic Biol Med 2011; 51: 993-9. doi: 10.1016/j. freeradbiomed.2010.12.005.
  • Nowotny K, Jung T, Höhn A, Weber D, Grune T. Advanced glycation end products and oxidative stress in type 2 diabetes mellitus. Biomolecules 2015; 5: 194-222. doi: 10.3390/ biom5010194.
  • Dornadula S, Elango B, Balashanmugam P, Palanisamy R, Kunka Mohanram R. Pathophysiological insights of methylglyoxal induced type-2 diabetes. Chem Res Toxicol 2015; 28: 1666-74. doi: 10.1021/acs.chemrestox.5b00171.
  • Lu J, Randell E, Han Y, Adeli K, Krahn J, Meng Q H. Increased plasma methylglyoxal level, inflammation, and vascular endothelial dysfunction in diabetic nephropathy. Clin Biochem 2011; 44: 307-11. doi: 10.1016/j. clinbiochem.2010.11.004.
  • Vicente Miranda H, Szego É M, Oliveira L M A, et al. Glycation potentiates α-synuclein-associated neurodegeneration in synucleinopathies. Brain 2017; 140: 1399-419. doi: 10.1093/ brain/awx056.
  • Biosa A, Outeiro T F, Bubacco L, Bisaglia M. Diabetes mellitus as a risk factor for Parkinson’s disease: a molecular point of view. Mol Neurobiol 2018; 55: 8754-63. doi: 10.1007/ s12035.018.1025-9.
  • Fitzmaurice A G, Rhodes S L, Lulla A, et al. Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease. Proc Natl Acad Sci U S A 2013; 110: 636- 41. doi: 10.1073/pnas.122.039.9110.
  • Zhang Z N, Zhang J S, Xiang J, et al. Subcutaneous rotenone rat model of Parkinson’s disease: Dose exploration study. Brain Res 2017; 1655: 104-13. doi: 10.1016/j.brainres.2016.11.020.
  • Meredith G E, Kang U J. Behavioral models of Parkinson’s disease in rodents: a new look at an old problem. Mov Disord 2006; 21: 1595-606. doi: 10.1002/mds.21010.
  • Fleming S M, Zhu C, Fernagut P O, et al. Behavioral and immunohistochemical effects of chronic intravenous and subcutaneous infusions of varying doses of rotenone. Exp Neurol 2004; 187: 418-29. doi: 10.1016/j. expneurol.2004.01.023.
  • Sharma M, Kaur J, Rakshe S, Sharma N, Khunt D, Khairnar A. Intranasal exposure to low-dose rotenone Induced alphasynuclein accumulation and Parkinson’s like symptoms without loss of dopaminergic neurons. Neurotox Res 2022; 40: 215-29. doi: 10.1007/s12640.021.00436-9.
  • Paxinos G, Watson C. The rat brain in stereotaxic coordinates. Hard cover 6th edition. Elsevier, 2006.
  • Bao L, Avshalumov M V, Rice M E. Partial mitochondrial inhibition causes striatal dopamine release suppression and medium spiny neuron depolarization via H2O2 elevation, not ATP depletion. J Neurosci 2005; 25: 10029-40. doi: 10.1523/ jneurosci.2652-05.2005.
  • Alam M, Danysz W, Schmidt W J, Dekundy A. Effects of glutamate and alpha2-noradrenergic receptor antagonists on the development of neurotoxicity produced by chronic rotenone in rats. Toxicol Appl Pharmacol 2009; 240: 198-207. doi: 10.1016/j.taap.2009.07.010.
  • Cenci M A, Francardo V, O’Sullivan S S, Lindgren H S. Rodent models of impulsive-compulsive behaviors in Parkinson’s disease: How far have we reached? Neurobiol Dis 2015; 82: 561-73. doi: 10.1016/j.nbd.2015.08.026.
  • Samii A, Nutt J G, Ransom B R. Parkinson’s disease. Lancet 2004; 363: 1783-93. doi: 10.1016/s0140-6736(04)16305-8.
  • Kravitz A V, Freeze B S, Parker P R, et al. Regulation of parkinsonian motor behaviours by optogenetic control of basal ganglia circuitry, Nature, 2010; 466: 622-6. doi: 10.1038/ nature09159.
  • Cataldi S, Stanley A T, Miniaci M C, Sulzer D. Interpreting the role of the striatum during multiple phases of motor learning. Febs j, 2022; 289: 2263-2281. doi: 10.1111/febs.15908.
  • Chegão A, Guarda M, Alexandre B M et al. Glycation modulates glutamatergic signaling and exacerbates Parkinson’s disease-like phenotypes, NPJ Parkinsons Dis 2022; 8: 51. doi: 10.1038/s41531.022.00314-x.
  • Panigrahi B, Martin K A, Li Y, et al. Dopamine is required for the neural representation and control of movement vigor. Cell, 2015; 162: 1418-30. doi: 10.1016/j.cell.2015.08.014.
  • Taylor T N, Greene J G, Miller G W. Behavioral phenotyping of mouse models of Parkinson’s disease. Behav Brain Res 2010; 211: 1-10. doi: 10.1016/j.bbr.2010.03.004.
  • Su R J, Zhen J L, Wang W, Zhang J L, Zheng Y, Wang X M. Timecourse behavioral features are correlated with Parkinson’s disease‑associated pathology in a 6-hydroxydopamine hemiparkinsonian rat model. Mol Med Rep 2018; 17: 3356-63. doi: 10.3892/mmr.2017.8277.
  • Lissner L J, Rodrigues L, Wartchow K M, et al. Shortterm alterations in behavior and astroglial function after intracerebroventricular infusion of methylglyoxal in rats. Neurochem Res 2021; 46: 183-96. doi: 10.1007/ s11064.020.03154-4.
  • Szczepanik J C, de Almeida G R L, Cunha M P, Dafre A L. Repeated methylglyoxal treatment depletes dopamine in the prefrontal cortex, and causes memory impairment and depressive-like behavior in mice, Neurochem Res 2020; 45: 354-70. doi: 10.1007/s11064.019.02921-2.
  • Hipkiss A R. On the relationship between energy metabolism, proteostasis, aging and Parkinson’s disease: Possible causative role of methylglyoxal and alleviative potential of carnosine. Aging Dis 2017; 8: 334-45. doi: 10.14336/ad.2016.1030.
  • Distler M G, Plant L D, Sokoloff G, et al. Glyoxalase 1 increases anxiety by reducing GABAA receptor agonist methylglyoxal. J Clin Invest 2012; 122: 2306-15. doi: 10.1172/jci61319.
  • Nehru B, Verma R, Khanna P, Sharma S K. Behavioral alterations in rotenone model of Parkinson’s disease: attenuation by co-treatment of centrophenoxine. Brain Res 2008; 1201: 122-7. doi: 10.1016/j.brainres.2008.01.074.
  • Palle S, Neerati P. Improved neuroprotective effect of resveratrol nanoparticles as evinced by abrogation of rotenoneinduced behavioral deficits and oxidative and mitochondrial dysfunctions in rat model of Parkinson’s disease. Naunyn Schmiedebergs Arch Pharmacol 2018; 391: 445-53. doi: 10.1007/s00210.018.1474-8.
  • Kandil E A, Abdelkader N F, El-Sayeh B M, Saleh S. Imipramine and amitriptyline ameliorate the rotenone model of Parkinson’s disease in rats. Neuroscience. 2016; 332: 26-37. doi: 10.1016/j.neuroscience.2016.06.040.
  • Greenamyre J T, Cannon J R, Drolet R, Mastroberardino P G. Lessons from the rotenone model of Parkinson’s disease. Trends Pharmacol Sci 2010; 31: 141-2; author reply 142-3. doi: 10.1016/j.tips.2009.12.006.
  • Khadrawy Y A, Salem A M, El-Shamy K A, Ahmed E K, Fadl N N, Hosny E N. Neuroprotective and therapeutic effect of caffeine on the rat model of Parkinson’s disease induced by rotenone. J Diet Suppl 2017; 14: 553-72. doi: 10.1080/19390.211.2016.1275916.
  • Greene J G, Noorian A R, Srinivasan S. Delayed gastric emptying and enteric nervous system dysfunction in the rotenone model of Parkinson’s disease. Exp Neurol 2009; 218: 154-61. doi: 10.1016/j.expneurol.2009.04.023.
  • Drolet R E, Cannon J R, Montero L, Greenamyre J T. Chronic rotenone exposure reproduces Parkinson’s disease gastrointestinal neuropathology. Neurobiol Dis 2009; 36: 96- 102. doi: 10.1016/j.nbd.2009.06.017.
  • Sharma N, Khurana N, Muthuraman A, Utreja P. Pharmacological evaluation of vanillic acid in rotenoneinduced Parkinson’s disease rat model. Eur J Pharmacol 2021; 903: 174112. doi: 10.1016/j.ejphar.2021.174112.
  • Ravenstijn P G, Merlini M, Hameetman M, et al. The exploration of rotenone as a toxin for inducing Parkinson’s disease in rats, for application in BBB transport and PK-PD experiments. J Pharmacol Toxicol Methods 2008; 57: 114-30. doi: 10.1016/j.vascn.2007.10.003.
  • Jia X, Olson D J, Ross A R, Wu L. Structural and functional changes in human insulin induced by methylglyoxal. Faseb J 2006; 20: 1555-7. doi: 10.1096/fj.05-5478fje.
  • Dhar A, Dhar I, Jiang B, Desai K M, Wu L. Chronic methylglyoxal infusion by minipump causes pancreatic betacell dysfunction and induces type 2 diabetes in Sprague- Dawley rats. Diabetes 2011; 60: 899-908. doi: 10.2337/db10- 0627.
  • Ankrah N A, Appiah-Opong R. Toxicity of low levels of methylglyoxal: depletion of blood glutathione and adverse effect on glucose tolerance in mice. Toxicol Lett 1999; 109: 61- 7. doi: 10.1016/s0378-4274(99)00114-9.
  • Matafome P, Santos-Silva D, Crisóstomo J, et al. Methylglyoxal causes structural and functional alterations in adipose tissue independently of obesity. Arch Physiol Biochem 2012; 118: 58-68. doi: 10.3109/13813.455.2012.658065.
Toplam 51 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Cerrahi (Diğer)
Bölüm Original Research
Yazarlar

Yekta Çulpan 0000-0001-7548-4095

Lara Ozden Bu kişi benim 0000-0001-8110-7691

Yakup Gozderesi 0000-0003-4229-6391

Beril Kocak Bu kişi benim 0009-0005-2046-865X

Zeynep Hazal Baltaci Bu kişi benim 0000-0002-6213-7286

Ayberk Denizli Bu kişi benim 0009-0004-3696-3412

Betul Yılmaz 0000-0003-1762-0284

Rezzan Gülhan 0000-0002-1519-3170

Yayımlanma Tarihi 31 Mayıs 2024
Gönderilme Tarihi 22 Aralık 2023
Kabul Tarihi 5 Ocak 2024
Yayımlandığı Sayı Yıl 2024

Kaynak Göster

APA Çulpan, Y., Ozden, L., Gozderesi, Y., Kocak, B., vd. (2024). Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model. Marmara Medical Journal, 37(2), 166-177. https://doi.org/10.5472/marumj.1480086
AMA Çulpan Y, Ozden L, Gozderesi Y, Kocak B, Baltaci ZH, Denizli A, Yılmaz B, Gülhan R. Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model. Marmara Med J. Mayıs 2024;37(2):166-177. doi:10.5472/marumj.1480086
Chicago Çulpan, Yekta, Lara Ozden, Yakup Gozderesi, Beril Kocak, Zeynep Hazal Baltaci, Ayberk Denizli, Betul Yılmaz, ve Rezzan Gülhan. “Effect of Methylglyoxal on Parkinson’s Disease Pathophysiology in the Rotenone Model”. Marmara Medical Journal 37, sy. 2 (Mayıs 2024): 166-77. https://doi.org/10.5472/marumj.1480086.
EndNote Çulpan Y, Ozden L, Gozderesi Y, Kocak B, Baltaci ZH, Denizli A, Yılmaz B, Gülhan R (01 Mayıs 2024) Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model. Marmara Medical Journal 37 2 166–177.
IEEE Y. Çulpan, L. Ozden, Y. Gozderesi, B. Kocak, Z. H. Baltaci, A. Denizli, B. Yılmaz, ve R. Gülhan, “Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model”, Marmara Med J, c. 37, sy. 2, ss. 166–177, 2024, doi: 10.5472/marumj.1480086.
ISNAD Çulpan, Yekta vd. “Effect of Methylglyoxal on Parkinson’s Disease Pathophysiology in the Rotenone Model”. Marmara Medical Journal 37/2 (Mayıs 2024), 166-177. https://doi.org/10.5472/marumj.1480086.
JAMA Çulpan Y, Ozden L, Gozderesi Y, Kocak B, Baltaci ZH, Denizli A, Yılmaz B, Gülhan R. Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model. Marmara Med J. 2024;37:166–177.
MLA Çulpan, Yekta vd. “Effect of Methylglyoxal on Parkinson’s Disease Pathophysiology in the Rotenone Model”. Marmara Medical Journal, c. 37, sy. 2, 2024, ss. 166-77, doi:10.5472/marumj.1480086.
Vancouver Çulpan Y, Ozden L, Gozderesi Y, Kocak B, Baltaci ZH, Denizli A, Yılmaz B, Gülhan R. Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model. Marmara Med J. 2024;37(2):166-77.