Effects of agomelatine in rotenone-induced Parkinson’s disease in rats

Günaydın, Caner; Avcı, Bahattin; Bozkurt, Ayhan; Önger, Mehmet Emin; Balci, Hakan; Bilge, S. Sırrı

doi:10.1016/j.neulet.2019.01.057

Cited by 16 publications

(6 citation statements)

References 38 publications

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“…Apomorphine is a nonselective dopamine agonist that activates both D1-like and D2-like receptors, and apomorphine-induced rotation in a rat model of PD is usually used to estimate the motor impairment (Xiong et al, 2009;Carbone et al, 2019;Gunaydin et al, 2019). At the end of the fourth week after rotenone-induced rat models of PD were established, a rotation test induced by apomorphine was performed.…”

Section: Effects Of Cory On Motor Dysfunction In the Rotenone-induced Animal Models Of Pdmentioning

confidence: 99%

Corynoxine Protects Dopaminergic Neurons Through Inducing Autophagy and Diminishing Neuroinflammation in Rotenone-Induced Animal Models of Parkinson’s Disease

Chen

Huang

et al. 2021

Front. Pharmacol.

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Recent studies have shown that impairment of autophagy is related to the pathogenesis of Parkinson’s disease (PD), and small molecular autophagy enhancers are suggested to be potential drug candidates against PD. Previous studies identified corynoxine (Cory), an oxindole alkaloid isolated from the Chinese herbal medicine Uncaria rhynchophylla (Miq.) Jacks, as a new autophagy enhancer that promoted the degradation of α-synuclein in a PD cell model. In this study, two different rotenone-induced animal models of PD, one involving the systemic administration of rotenone at a low dosage in mice and the other involving the infusion of rotenone stereotaxically into the substantia nigra pars compacta (SNpc) of rats, were employed to evaluate the neuroprotective effects of Cory. Cory was shown to exhibit neuroprotective effects in the two rotenone-induced models of PD by improving motor dysfunction, preventing tyrosine hydroxylase (TH)-positive neuronal loss, decreasing α-synuclein aggregates through the mechanistic target of the rapamycin (mTOR) pathway, and diminishing neuroinflammation. These results provide preclinical experimental evidence supporting the development of Cory into a potential delivery system for the treatment of PD.

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Section: Effects Of Cory On Motor Dysfunction In the Rotenone-induced Animal Models Of Pdmentioning

confidence: 99%

Corynoxine Protects Dopaminergic Neurons Through Inducing Autophagy and Diminishing Neuroinflammation in Rotenone-Induced Animal Models of Parkinson’s Disease

Chen

Huang

et al. 2021

Front. Pharmacol.

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“…Rotenone, a naturally derived pesticide, acts as a specific mitochondrial complex1 inhibitor and induces oxidative stress by increasing the formation of reactive oxygen species by its prominent mitochondrial complex inhibition and impaired ATP production. Evidence suggests that rotenone-induced PD is a suitable model as it simulates the behavioral and neuropathological features of disease due to selective degeneration of dopaminergic neurons (28)(29)(30). Oxidative stress may play a greater role in the demise of dopaminergic neurons indirectly by activating intracellular, cell death-related molecular pathways (30,31).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of methanolic extract of Sargassum wightii on rotenone-induced parkinsonism-like symptoms in Wistar albino rats

Rout

Rath

Bhattamisra

et al. 2021

J Herbmed Pharmacol

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Introduction: The pathogenesis of Parkinson’s disease (PD) is multifactorial in which oxidative stress, neuroinflammation, and mitochondrial dysfunction are the leading factors. Currently, the antioxidant and anti-inflammatory agents of natural sources as neuroprotectants have raised much attention. The current study aimed to explore the neuroprotective effect of methanolic extract of Sargassum wightii in male Wistar albino rats against rotenone-induced PD. Methods: The rats were administered with rotenone (10 mg/kg orally) daily for 28 days to induce PD. S. wightii (200 mg/kg and 400 mg/kg) and levodopa+carbidopa combination (10 mg/kg) were administered to different groups of rats one hour prior to rotenone for 28 days. Behavioral parameters (akinesia, tremor, motor coordination, and locomotor activities) and body weight were recorded on days 14th and 28th of drug treatment. On the 28th day, the animals were sacrificed for the neurobiochemical analyses of brain tissue. Results: Rotenone treatment caused a significant reduction in behavioural parameters (P < 0.001), neurochemical deficits (P < 0.001), and elevation of oxidative stress markers (P < 0.001) in the brain. Pre-treatment with S. wightii at 200 mg/kg and 400 mg/kg doses significantly attenuated the rotenone-induced behavioral alterations and restored the mitochondrial NADH dehydrogenase activity and dopamine level in the striatum (P < 0.001). Moreover, 400 mg/kg of S. wightii restored the rotenone-induced increased oxidative stress markers like malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) in the striatum (P < 0.01). Conclusion: S. wightii has provided a neuroprotective effect, probably by virtue of its antioxidant and dopamine restoring potential. Hence, it may offer a promising and new therapeutic lead for the treatment of PD but needs further research.

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“…Günaydın ve ark. (21) Sprague-Dawley sıçanlarda rotenon ile oluşturulmuş olan PH modelinde 18 gün süreli 40 mg/kg peroral agomelatin tedavisinin kaspaz 3 aracılı apoptosisi indükleyerek striatal nöron sayısında azalmaya neden olduğunu göstermişlerdir. Agomelatin ayrıca her iki testte de sıçanların motor fonksiyonlarını kötüleştirmiştir.…”

Section: Discussionunclassified

Agomelatin’s Effect on Parkinson Disease Model on Rats

Soner¹,

Ayvat²,

Şahin³

2019

BUCH

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Parkinson hastalığı en sık görülen nörodejeneratif hastalıklardan biridir. Günümüzde hastalığın tam tedavisi bulunmamaktadır. Agomelatin pineal bezde sentezlenip salıverilen melatonin hormonunun sentetik analoğudur; merkezi sinir sistemindeki (MSS) antidepresan etkilerini melatonin kaynaklı MT1 ve MT2 reseptörlerini aktive ederek, monoamin kaynaklı serotonin 5-HT2C reseptörlerini antagonize ederek gösterir. Çalışmamızda, oral Agomelatin uygulamasının sıçanlarda 6-OHDA ile oluşturulan deneysel Parkinson hastalığı üzerine etkilerini araştırdık. Yöntem: Bu amaçla 270-330 g aralığında üç gruptaki 45 sıçana unilateral intrastriatal 6-OHDA uygulandı. Kontrol grubuna çözücü, tedavi gruplarına ise 5 mg/kg/gün ve 20 mg/kg/gün Agomelatin tedavisi 15 gün süre ile uygulandı. Bu süre sonunda motor koordinasyon ve beceriler yapışkan bant testi, açık alan testi ve silindir testi ile değerlendirilirken, dopaminerjik hasar derecesi apomorfin ile indüklenen dönme testi ile değerlendirildi. Bulgular: Çalışmamızda, her iki dozda uygulanan Agomelatinin, (5 mg/kg ve 20 mg/kg) 6-OHDA aracılı oluşturulan deneysel Parkinson hastalığında progresyonu önlediğini saptadık. Sonuç: Agomelatin deneysel Parkinson hastalığı modelinde striatal nöronlardaki hasar üzerine koruyucu etki göstermiştir.

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Effects of agomelatine in rotenone-induced Parkinson’s disease in rats

Cited by 16 publications

References 38 publications

Corynoxine Protects Dopaminergic Neurons Through Inducing Autophagy and Diminishing Neuroinflammation in Rotenone-Induced Animal Models of Parkinson’s Disease

Corynoxine Protects Dopaminergic Neurons Through Inducing Autophagy and Diminishing Neuroinflammation in Rotenone-Induced Animal Models of Parkinson’s Disease

Neuroprotective effect of methanolic extract of Sargassum wightii on rotenone-induced parkinsonism-like symptoms in Wistar albino rats

Agomelatin’s Effect on Parkinson Disease Model on Rats

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