Effect of cerebrolysin on dopaminergic neurodegeneration of rat with oxidative stress induced by 3-nitropropionic acid

Guzmán, David Calderón; Brizuela, Norma Osnaya; Herrera, Maribel Ortíz; García, Ernestina Hernández; Mejía, Gerardo Barragán; Olguı́n, Hugo Juárez; Peraza, Armando Valenzuela; Attilus, Jonas; Ruíz, Norma Labra

doi:10.1515/acph-2016-0027

Cited by 10 publications

(4 citation statements)

References 12 publications

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“…Our study suggested that cerebroprotein hydrolysates also played an important role in improving ferroptosis in nerve cells, and the potential mechanism of inhibiting ferroptosis-related peroxidation. These findings were consistent with previous research that cerebroprotein hydrolysate can effectively improve oxidative stress and reduce lipid peroxidation in models of nerve damage induced by hypoglycaemia ( Patocková et al, 2003 ), 3-nitropropionic acid ( Calderón Guzmán et al, 2016 ), chronic alcoholism ( Vaghef et al, 2019 ), etc.…”

Section: Discussionsupporting

confidence: 92%

Cerebroprotein hydrolysate attenuates neurodegenerative changes in Alzheimer’s mice model via ferroptosis pathway

Chen

Song

Chen³

et al. 2023

Front. Pharmacol.

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Introduction: Cerebroprotein hydrolysate has been proven to improve cognitive function in patients with Alzheimer’s disease (AD). We explored the safety and effectiveness of the clinical administration of oral cerebroprotein hydrolysate in AD, and possible mechanisms related to the neuronal ferroptosis pathway.Methods: Three-month-old male APP/PS1 double-transgenic mice were randomly divided into AD model (n = 8) and intervention (n = 8) groups. Eight non-transgenic wild-type (WT) C57 mice were used as age-matched controls. The experiments were started at the age of 6 months. The intervention group was then administered cerebroprotein hydrolysate nutrient solution (11.9 mg/kg/day) via chronic gavage, the other groups received an identical volume of distilled water. Behavioural experiments were performed after 90 days of continuous administration. Serum and hippocampal tissues were then collected for histomorphological observation, tau and p-tau expression, and ferroptosis markers analysis.Results: Cerebroprotein hydrolysate simplified movement trajectories and shortened escape latencies of APP/PS1 mice in the Morris water maze test. Neuronal morphologies were restored in hippocampal tissues on haematoxylin-eosin staining. In the AD-model group, Aβ protein and p-tau/tau expression levels were elevated, plasma Fe2+ and malondialdehyde levels were elevated, GXP4 protein expression and plasma glutathione levels declined than controls. All indices improved after cerebroprotein hydrolysate intervention.Conclusion: Cerebroprotein hydrolysate improves learning and memory function, alleviates neuronal damage, and reduces the deposition of pathological AD markers in AD mice, which may be related to the inhibition of neuronal ferroptosis.

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Section: Discussionsupporting

confidence: 92%

Cerebroprotein hydrolysate attenuates neurodegenerative changes in Alzheimer’s mice model via ferroptosis pathway

Chen

Song

Chen³

et al. 2023

Front. Pharmacol.

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“…ROS, caused by oxidative stress, lead to lipid peroxidation as well as protein oxidation, resulting in plasma membrane broken and cross-linking of cytoskeletal biomolecules [33][34][35][36]. Antioxidants can reduce or delay oxidation process though preventing the initiation or propagation of oxidizing chain reactions.…”

Section: Discussionmentioning

confidence: 99%

Berberine Protects against Hydrogen Peroxide-Induced Oxidative Damage in PC12 Cells through Activation of ERK1/2 Pathway

Liu¹,

Zeng²,

Gaur³

et al. 2017

Clin Exp Pharmacol

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Oxidative stress is a much-recognized phenomenon linked with the progression of Neurodegenerative Diseases (NDs) due to imbalances in redox homeostasis. Increasing evidence indicates that excessive Reactive Oxygen Species (ROS), impairing the physiological functions of neurons via inducing cell apoptosis, is the main cause of NDs. The drug candidates are required that can effectively protect neurons from oxidative stress insult to slow down the process of neurodegenerative diseases. In present study, we investigated the protective effect and the underlying mechanisms of berberine (BBR, an isoquinoline alkaloid isolated from the herb Rhizoma coptidis, against oxidative damage in PC12 cells. It was found that BBR was able to suppress hydrogen peroxide (H 2 O 2 )-induced cell death in PC12 cells. Flow cytometry revealed that BBR significantly reduced the apoptosis of PC12 cells exposed to H 2 O 2 . Western blot analysis displayed that BBR stimulated the extracellular regulated ERK1/2 survival signaling, while application of PC12 cells with ERK1/2 pathway inhibitor PD98059 blocked the neuroprotective effect of BBR. These results together indicated that BBR is a potential protectant, and it protects PC12 cells against H 2 O 2 toxicity through activated the ERK1/2 pathway.

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“…Oxidative stress, caused by the overproduction of ROS leads to lipid peroxidation, protein oxidation, plasma membrane breakage as well as cross-linking of cytoskeletal biomolecules, which play a key role in the pathogenesis of AD [29][30][31][32]. Increasing evidences support that antioxidants extracted from the plants can reduce or delay oxidation process [1].…”

Section: Discussionmentioning

confidence: 99%

The p38-MAPK Pathway Is Involved in Neuroprotection of Artemisinin against H2O2-induced Apoptosis in PC12 Cells

Liu¹,

Zeng²,

Gaur³

et al. 2017

JPP

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Oxidative stress, owing to the excessive production of ROS (reactive oxygen species), is one of the leading causes for the progression of AD (Alzheimer's disease). Increasing evidences suggested that oxidative stress insult impaired the physiological functioning of neuronal cells by inducing cell apoptosis. The search for drug candidates that can effectively protect neurons from oxidative stress insult might hold therapeutic potential for AD. In the present study, we tested the neuroprotective effects and the related action mechanisms of artemisinin, a FDA-approved anti-malarial drug, against H 2 O 2 induced oxidative damage in PC12 cells. It was found that artemisinin reduced cell viability loss caused by hydrogen peroxide (H 2 O 2 ) in PC12 cells. In addition, data from Flow cytometry displayed that artemisinin significantly decreased the apoptosis of PC12 cells induced by H 2 O 2 . Furthermore Western blot analysis displayed that artemisinin stimulated the p38MAPK signaling, while treatment of PC12 cells with specific p38MAPK pathway inhibitor SB203580 blocked the neuroprotective effect of artemisinin. These results together indicated that artemisinin is a potential protectant, and it protects PC12 cells against H 2 O 2 injury through activation of the p38MAPK pathway.

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Effect of cerebrolysin on dopaminergic neurodegeneration of rat with oxidative stress induced by 3-nitropropionic acid

Cited by 10 publications

References 12 publications

Cerebroprotein hydrolysate attenuates neurodegenerative changes in Alzheimer’s mice model via ferroptosis pathway

Cerebroprotein hydrolysate attenuates neurodegenerative changes in Alzheimer’s mice model via ferroptosis pathway

Berberine Protects against Hydrogen Peroxide-Induced Oxidative Damage in PC12 Cells through Activation of ERK1/2 Pathway

The p38-MAPK Pathway Is Involved in Neuroprotection of Artemisinin against H2O2-induced Apoptosis in PC12 Cells

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