Imipramine and amitriptyline ameliorate the rotenone model of Parkinson’s disease in rats

Kandil, Esraa A.; Abdelkader, Noha F.; El-Sayeh, Bahia M.; Saleh, S. A.

doi:10.1016/j.neuroscience.2016.06.040

Cited by 45 publications

(23 citation statements)

References 69 publications

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“…PD is the second most common neurodegenerative disease and is characterized by a loss of dopaminergic neurons . Some environmental risk factors, such as ROT and MPP + , are used as neurotoxins for evaluating potential neuroprotective strategies against apoptotic diseases like PD . For in vitro PD studies, the SH‐SY5Y human neuroblastoma cell line is frequently used as a cell model, because it exhibits many characteristics of dopaminergic neurons .…”

Section: Discussionmentioning

confidence: 99%

“…24,25 Some environmental risk factors, such as ROT and MPP + , are used as neurotoxins for evaluating potential neuroprotective strategies against apoptotic diseases like PD. [26][27][28][29][30] For in vitro PD studies, the SH-SY5Y human neuroblastoma cell line is frequently used as a cell model, because it exhibits many characteristics of dopaminergic neurons. 31,32 In the present study, we demonstrated that both RBM3 and mild hypothermia protect SH-SY5Y cells from ROT-induced neurotoxicity.…”

Section: Discussionmentioning

confidence: 99%

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Cold‐inducible protein RBM3 mediates hypothermic neuroprotection against neurotoxin rotenone via inhibition on MAPK signalling

Yang

Zhuang

et al. 2019

J Cellular Molecular Medi

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Mild hypothermia and its key product, cold‐inducible protein RBM3, possess robust neuroprotective effects against various neurotoxins. However, we previously showed that mild hypothermia fails to attenuate the neurotoxicity from MPP+, one of typical neurotoxins related to the increasing risk of Parkinson disease (PD). To better understand the role of mild hypothermia and RBM3 in PD progression, another known PD‐related neurotoxin, rotenone (ROT) was utilized in this study. Using immunoblotting, cell viability assays and TUNEL staining, we revealed that mild hypothermia (32°C) significantly reduced the apoptosis induced by ROT in human neuroblastoma SH‐SY5Y cells, when compared to normothermia (37°C). Meanwhile, the overexpression of RBM3 in SH‐SY5Y cells mimicked the neuroprotective effects of mild hypothermia on ROT‐induced cytotoxicity. Upon ROT stimulation, MAPK signalling like p38, JNK and ERK, and AMPK and GSK‐3β signalling were activated. When RBM3 was overexpressed, only the activation of p38, JNK and ERK signalling was inhibited, leaving AMPK and GSK‐3β signalling unaffected. Similarly, mild hypothermia also inhibited the activation of MAPKs induced by ROT. Lastly, it was demonstrated that the MAPK (especially p38 and ERK) inhibition by their individual inhibitors significantly decreased the neurotoxicity of ROT in SH‐SY5Y cells. In conclusion, these data demonstrate that RBM3 mediates mild hypothermia‐related neuroprotection against ROT by inhibiting the MAPK signalling of p38, JNK and ERK.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cold‐inducible protein RBM3 mediates hypothermic neuroprotection against neurotoxin rotenone via inhibition on MAPK signalling

Yang

Zhuang

et al. 2019

J Cellular Molecular Medi

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“…Group II received ABZ (10 mg/kg/day, orally) starting from the 11th day to serve as ABZ control group . Group III was injected with rotenone (1.5 mg/kg/48 hours, subcutaneously) for 21 days . Group IV received rotenone as in group III and ABZ as in group II 1 h before rotenone injection (Figure ).…”

Section: Methodsmentioning

confidence: 99%

Hypoxia‐inducible factor 1 alpha and nuclear‐related receptor 1 as targets for neuroprotection by albendazole in a rat rotenone model of Parkinson's disease

Kandil

Sayed

Ahmed

et al. 2019

Clin Exp Pharma Physio

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Abbreviations: ABZ, albendazole; CoREST, corepressor for repressor element 1 silencing transcription factor; DA, dopamine; GDNF, glial cell line-derived neurotrophic factor; HIF-1α, hypoxia-inducible factor-1 alpha; NF-кB, nuclear factor kappa beta; Nurr1, nuclear receptor related 1; PD, Parkinson's disease; SN, substantia nigra; TH, tyrosine hydroxylase; TNF-α, tumor necrosis factor alpha; VEGF, vascular endothelial growth factor; VMAT, vesicular monoamine transporter. AbstractHypoxia-inducible factor-1 alpha (HIF-1α) and nuclear receptor related-1 (Nurr1) play pivotal roles in the development and survival of dopaminergic neurons, and deficiencies in these genes may be involved in Parkinson's disease (PD) pathogenesis.Recently, anthelminthic benzimidazoles were shown to promote HIF-1α transcription in vitro and were proposed to activate Nurr1 via their benzimidazole group.Therefore, the aim of this study was to explore the neuroprotective effects of albendazole (ABZ), an anthelminthic benzimidazole, in a rotenone model of Parkinson's disease (PD). Rotenone (1.5 mg/kg) was subcutaneously injected into rats every other day for a period of 21 days, resulting in the development of the essential features of PD. In addition to rotenone, ABZ (10 mg/kg) was administered orally starting from the 11th day. Treatment of rats with ABZ markedly mitigated rotenone-induced histological alterations in substantia nigra (SN), restored striatal dopamine (DA) level and motor functions and decreased the expression of α-synuclein (a disease marker protein). ABZ also enhanced expression of Hypoxia-inducible factor-1 alpha (HIF-1α) in the SN along with its downstream target, vascular endothelial growth factor, promoting neuronal survival. Similarly, ABZ augmented nuclear receptor related-1 (Nurr1) expression in the SN and increased transcriptional activation of Nurr1-controlled genes, which are essential for regulation of DA synthesis; additionally, expression of neurotoxic proinflammatory cytokines that induce neuronal death was suppressed.In conclusion, the present study suggests that ABZ exerts a neuroprotective effect in a rotenone-induced PD model associated with HIF-1α and Nurr1 activation and thus may be a viable candidate for treating PD.

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“…Imipramine [247] Isobavachalcone [248] Isochlorogenic acid [167] Isoquercetin (Isoquercitrin) [249] Kaempferol [128,160,193,194] Kaempferol, 3-O-a-l arabinofuranoside-7-O-a-l-rhamnopyranoside [214] KR33493 [250] Kukoamine [251] Lestaurtinib [164] Lipoic acid [252][253][254] Luteolin [128] LY354740 [115] M10 [24] M30 (VAR10303) [112,255] M99 [24] Macranthoin G [256] Magnesium lithospermate B [257] [160,193,194,267] [18F]MPPF [107] MSX-3 [268] Myricetin [128,269,270] Myricitrin [271] Naringenin [128,272] Naringin [117,273,274] Nicotinamide adenine dinucleotide phosphate (NADPH) [275,276] Nicotinamide mononucleotide [277] Nitecapone [278] Nordihydroguaiaretic [160,193,194] Oleuropein…”

Section: Compound Name(s) Referencesmentioning

confidence: 99%

Metal Chelation Therapy and Parkinson’s Disease: A Critical Review on the Thermodynamics of Complex Formation between Relevant Metal Ions and Promising or Established Drugs

Tosato

Marco

2019

Biomolecules

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The present review reports a list of approximately 800 compounds which have been used, tested or proposed for Parkinson’s disease (PD) therapy in the year range 2014–2019 (April): name(s), chemical structure and references are given. Among these compounds, approximately 250 have possible or established metal-chelating properties towards Cu(II), Cu(I), Fe(III), Fe(II), Mn(II), and Zn(II), which are considered to be involved in metal dyshomeostasis during PD. Speciation information regarding the complexes formed by these ions and the 250 compounds has been collected or, if not experimentally available, has been estimated from similar molecules. Stoichiometries and stability constants of the complexes have been reported; values of the cologarithm of the concentration of free metal ion at equilibrium (pM), and of the dissociation constant Kd (both computed at pH = 7.4 and at total metal and ligand concentrations of 10–6 and 10–5 mol/L, respectively), charge and stoichiometry of the most abundant metal–ligand complexes existing at physiological conditions, have been obtained. A rigorous definition of the reported amounts is given, the possible usefulness of this data is described, and the need to characterize the metal–ligand speciation of PD drugs is underlined.

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Imipramine and amitriptyline ameliorate the rotenone model of Parkinson’s disease in rats

Cited by 45 publications

References 69 publications

Cold‐inducible protein RBM3 mediates hypothermic neuroprotection against neurotoxin rotenone via inhibition on MAPK signalling

Cold‐inducible protein RBM3 mediates hypothermic neuroprotection against neurotoxin rotenone via inhibition on MAPK signalling

Hypoxia‐inducible factor 1 alpha and nuclear‐related receptor 1 as targets for neuroprotection by albendazole in a rat rotenone model of Parkinson's disease

Metal Chelation Therapy and Parkinson’s Disease: A Critical Review on the Thermodynamics of Complex Formation between Relevant Metal Ions and Promising or Established Drugs

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