Ramelteon ameliorated 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity in neuronal cells in a mitochondrial-dependent pathway

Li, Chuo; Zhang, Yusheng; Liu, Rongrong; Mai, Yuzhen

doi:10.1080/21655979.2021.1960767

Cited by 7 publications

(6 citation statements)

References 38 publications

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“…However, mitochondrial dysfunction results in upregulation of proapoptotic factor which triggers the activation of caspase 3, leading to the neuronal cell death 74 . Bcl-2 family members can also be activated by BDNF as reported in MPP + -induced neuronal cell line SH-SY5Y cells and mouse models 75 . Similarly, our Western blotting experiment revealed a decrease in the ratio of Bax/Bcl-2 and cleaved Caspase3 in the rotenone induced mouse model due to abrupt increase in ROS level that resulted in uncontrolled series of apoptosis.…”

Section: Discussionmentioning

confidence: 81%

Oleuropein confers neuroprotection against rotenone-induced model of Parkinson’s disease via BDNF/CREB/Akt pathway

Zahra

Singh

Birla

et al. 2023

Sci Rep

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Major pathological features of Parkinson’s disease (PD) include increase in oxidative stress leading to the aggregation of α-synuclein, mitochondrial dysfunction and apoptosis of dopaminergic neurons. In addition, downregulation of the expression of neurotrophic factors like-Brain Derived Neurotrophic Factor (BDNF) is also involved in PD progression. There has been a lot of interest in trophic factor-based neuroprotective medicines over the past few decades to treat PD symptoms. Rotenone, an insecticide, inhibits the mitochondrial complex I causing overproduction of ROS, oxidative stress, and aggregation of α-synuclein. It has been shown that BDNF and Tropomyosin receptor kinase B (TrkB) interaction initiates the regulation of neuronal cell development and differentiation by the serine/threonine protein kinases like Akt and GSK-3β. Additionally, Transcription factor CREB (cAMP Response Element-binding protein) also determines the gene expression of BDNF. The homeostasis of these signalling cascades is compromised with the progression of PD. Therefore, maintaining the equilibrium of these signalling cascades will delay the onset of PD. Oleuropein (OLE), a polyphenolic compound present in olive leaves has been documented to cross blood brain barrier and shows potent antioxidative property. In the present study, the dose of 8, 16 and 32 mg/kg body weight (bwt) OLE was taken for dose standardisation. The optimised doses of 16 and 32 mg/kg bwt was found to be neuroprotective in Rotenone induced PD mouse model. OLE improves motor impairment and upregulate CREB regulation along with phosphorylation of Akt and GSK-3β in PD mouse. In addition, OLE also reduces the mitochondrial dysfunction by activation of enzyme complexes and downregulates the proapoptotic markers in Rotenone intoxicated mouse model. Overall, our study suggests that OLE may be used as a therapeutic agent for treatment of PD by regulating BDNF/CREB/Akt signalling pathway.

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Section: Discussionmentioning

confidence: 81%

Oleuropein confers neuroprotection against rotenone-induced model of Parkinson’s disease via BDNF/CREB/Akt pathway

Zahra

Singh

Birla

et al. 2023

Sci Rep

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“…Therefore, the inhibition of astrocyte reactivity may be a potential neuroprotective target. Oxidative stress and hypoxia have been proven to play a critical role in the process of neurodegeneration in various neurological disorders, such as amyotrophic lateral sclerosis (ALS), PD and AD [ 27 , 28 , 29 ]. Oxidized free radicals at high concentrations are extremely reactive and damage neurons in CNS [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Nobiletin Alleviates Astrocyte Activation and Oxidative Stress Induced by Hypoxia In Vitro

Wang

Gao

et al. 2022

Molecules

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Increasing evidence indicates that nobiletin (NOB) is a promising neuroprotective agent. Astrocyte activation plays a key role in neurodegenerative disorders. Thus, this study aims to investigate the effects of NOB on astrocyte activation and the potential mechanisms. In this study, astrocytes were exposed to hypoxia injury for 24 h to induce activation in vitro. Glial fibrillary acidic protein (GFAP) was chosen as a marker of astrocyte activation. To evaluate the effects of NOB on the migration of activated astrocytes, we used a scratch wound healing assay and Transwell migration assay. In addition, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), mitochondrial membrane potential, Nrf2 and HO-1 were measured to investigate the mechanisms of NOB in the activation of astrocytes. We found that NOB alleviated astrocyte activation and decreased GFAP expression during hypoxia. Simultaneously, NOB alleviated the migration of astrocytes induced by hypoxia. With NOB treatment, hypoxia-induced oxidative stress was partially reversed, including reducing the production of ROS and MDA. Furthermore, NOB significantly improved the mitochondrial dysfunction in activated astrocytes. Finally, NOB promoted Nrf2 nuclear translocation and HO-1 expression in response to continuous oxidative damage. Our study indicates, for the first time, that NOB alleviates the activation of astrocytes induced by hypoxia in vitro, in part by ameliorating oxidative stress and mitochondrial dysfunction. This provides new insights into the neuroprotective effects of NOB.

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“…The effect of cadmium on the mitochondria has been considered as the main cause of cell apoptosis [ 35 , 36 ]. Regarding the mechanism of cell apoptosis, abnormal mitochondrial function is an important pathway [ 37 , 38 ]. The damage of mitochondrial inner membrane can be accompanied by the release of apoptotic induction factor and Caspase proteinase in the mitochondrial membrane gap, which causes apoptosis through the cascade reaction of apoptosis [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Role of Fucoxanthin towards Cadmium-induced renal impairment with the antioxidant and anti-lipid peroxide activities

et al. 2021

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Kidney damages caused by cadmium are considered to be one of the most dangerous consequences for the human body. This study aimed to investigate the protective effects of fucoxanthin supplementation on mice models subjected to cadmium-induced kidney damage. The mice treated with cadmium chloride (CdCl 2 ) were observed to have significantly reduced the crosssection area of glomeruli. Cadmium exposure has also caused the damage of the structural integrity of mitochondria and increased blood urea nitrogen (BUN), kidney injury molecule 1 (KIM1), and neutrophil gelatinase associated lipocalin (NGAL) levels. Peroxidase (POD), superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) levels in cadmium-exposed mice were markedly declined. Caspase3, caspase8, and caspase9 gene expressions in association with apoptosis were dramatically elevated in renal tissues. The CdCl 2 treated mice were orally administered with 50 mg/kg Shenfukang, 10 mg/kg, 25 mg/kg, and 50 mg/kg fucoxanthin for 14 days. The results revealed that high doses of fucoxanthin administration significantly decreased BUN, KIM1, NGAL levels, increasing POD, SOD, CAT, and ascorbate APX levels. Fucoxanthin administration also promoted recovery of the renal functions, micro-structural organization, and ultrastructural organization in the renal cells. In summary, the ameliorative effects of fucoxanthin supplementation against cadmium-induced kidney damage were mediated via inhibiting oxidative stress and apoptosis, promoting the recovery of structural integrity of mitochondria.

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Ramelteon ameliorated 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity in neuronal cells in a mitochondrial-dependent pathway

Cited by 7 publications

References 38 publications

Oleuropein confers neuroprotection against rotenone-induced model of Parkinson’s disease via BDNF/CREB/Akt pathway

Oleuropein confers neuroprotection against rotenone-induced model of Parkinson’s disease via BDNF/CREB/Akt pathway

Nobiletin Alleviates Astrocyte Activation and Oxidative Stress Induced by Hypoxia In Vitro

Role of Fucoxanthin towards Cadmium-induced renal impairment with the antioxidant and anti-lipid peroxide activities

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