Salidroside Protects against MPP+‐Induced Neuronal Injury through DJ‐1‐Nrf2 Antioxidant Pathway

Wu, Leitao; Xu, Hang; Cao, Liang; Li, Tao; Li, Ruru; Feng, Yunjiang; Chen, Jianzong; Ma, Jing

doi:10.1155/2017/5398542

Cited by 16 publications

(12 citation statements)

References 42 publications

(36 reference statements)

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“…DJ-1 acts as a chaperone and protease to stabilize mitochondria and protect cells from oxidative stress ( 344 ). Several other cellular functions have been attributed to DJ-1, including; binding of Ras as a transcriptional co-activator ( 345 ), negative regulation of the phosphoinositide-3-kinase (PI3K)/AKT signaling cascade through inhibition of PTEN ( 309 , 346 , 347 ), chaperone function ( 348 , 349 ), and RNA binding ( 350 ). Although controversial, DJ-1 has also been claimed to have glyoxalase ( 351 ) and deglycase ( 352 ) enzyme activities ( 353 ).…”

Section: Metformin: Mechanism Of Action In Neurodegenerative Diseasesmentioning

confidence: 99%

The Therapeutic Potential of Metformin in Neurodegenerative Diseases

2018

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The search for treatments for neurodegenerative diseases is a major concern in light of today's aging population and an increasing burden on individuals, families, and society. Although great advances have been made in the last decades to understand the underlying genetic and biological cause of these diseases, only some symptomatic treatments are available. Metformin has long since been used to treat Type 2 Diabetes and has been shown to be beneficial in several other conditions. Metformin is well-tested in vitro and in vivo and an approved compound that targets diverse pathways including mitochondrial energy production and insulin signaling. There is growing evidence for the benefits of metformin to counteract age-related diseases such as cancer, cardiovascular disease, and neurodegenerative diseases. We will discuss evidence showing that certain neurodegenerative diseases and diabetes are explicitly linked and that metformin along with other diabetes drugs can reduce neurological symptoms in some patients and reduce disease phenotypes in animal and cell models. An interesting therapeutic factor might be how metformin is able to balance survival and death signaling in cells through pathways that are commonly associated with neurodegenerative diseases. In healthy neurons, these overarching signals keep energy metabolism, oxidative stress, and proteostasis in check, avoiding the dysfunction and neuronal death that defines neurodegenerative disease. We will discuss the biological mechanisms involved and the relevance of neuronal vulnerability and potential difficulties for future trials and development of therapies.

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Section: Metformin: Mechanism Of Action In Neurodegenerative Diseasesmentioning

confidence: 99%

The Therapeutic Potential of Metformin in Neurodegenerative Diseases

2018

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“… 29 , 52 More recently, salidroside (25–100 μM) was also reported to significantly reduce MPP + -induced neuronal injury via DJ-1 -Nrf2 antioxidant pathway in SH-SY5Y cells. 53 Besides, it was demonstrated that salidroside (100 μg/mL) could induce the differentiation of rat mesenchymal stem cells (MSCs) to dopaminergic neurons with increased DA release. 54 Salidro-side was also reported to protect primary cortical neurons and SN4741 cells from endoplasmic reticulum (ER) stress.…”

Section: Pharmacological Activity and Mechanisms Of Actionmentioning

confidence: 99%

Pharmacological activities, mechanisms of action, and safety of salidroside in the central nervous system

Zhong¹,

Han²,

Zhang³

et al. 2018

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The primary objective of this review article was to summarize comprehensive information related to the neuropharmacological activity, mechanisms of action, toxicity, and safety of salidroside in medicine. A number of studies have revealed that salidroside exhibits neuroprotective activities, including anti-Alzheimer’s disease, anti-Parkinson’s disease, anti-Huntington’s disease, anti-stroke, anti-depressive effects, and anti-traumatic brain injury; it is also useful for improving cognitive function, treating addiction, and preventing epilepsy. The mechanisms underlying the potential protective effects of salidroside involvement are the regulation of oxidative stress response, inflammation, apoptosis, hypothalamus-pituitary-adrenal axis, neurotransmission, neural regeneration, and the cholinergic system. Being free of side effects makes salidroside potentially attractive as a candidate drug for the treatment of neurological disorders. It is evident from the available published literature that salidroside has potential use as a beneficial therapeutic medicine with high efficacy and low toxicity to the central nervous system. However, the definite target protein molecules remain unclear, and clinical trials regarding this are currently insufficient; thus, guidance for further research on the molecular mechanisms and clinical applications of salidroside is urgent.

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“…ARE is located in the promoter region of several genes encoding various antioxidant enzymes [ 78 ]. Silencing of Nrf2 significantly inhibits mRNA and protein expression of SOD1, and SOD2 [ 79 ]. We suppose that degradation of Nrf2 via the phosphorylation by GSK-3β may lead to a similar result ( Figure 3 ).…”

Section: Suggestions Of Pi3k/akt/pten Signaling On Sod Expressionmentioning

confidence: 99%

Implications of PI3K/AKT/PTEN Signaling on Superoxide Dismutases Expression and in the Pathogenesis of Alzheimer’s Disease

et al. 2018

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Alzheimer’s disease is a neurodegenerative sickness, where the speed of personal disease progression differs prominently due to genetic and environmental factors such as life style. Alzheimer’s disease is described by the construction of neuronal plaques and neurofibrillary tangles composed of phosphorylated tau protein. Mitochondrial dysfunction may be a noticeable feature of Alzheimer’s disease and increased production of reactive oxygen species has long been described. Superoxide dismutases (SODs) protect from excess reactive oxygen species to form less reactive hydrogen peroxide. It is suggested that SODs can play a protective role in neurodegeneration. In addition, PI3K/AKT pathway has been shown to play a critical role on the neuroprotection and inhibiting apoptosis via the enhancing expression of the SODs. This pathway appears to be crucial in Alzheimer’s disease because it is related to the tau protein hyper-phosphorylation. Dietary supplementation of several ordinary compounds may provide a novel therapeutic approach to brain disorders by modulating the function of the PI3K/AKT pathway. Understanding these systems may offer a better efficacy of new therapeutic approaches. In this review, we summarize recent progresses on the involvement of the SODs and PI3K/AKT pathway in neuroprotective signaling against Alzheimer’s disease.

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Salidroside Protects against MPP+‐Induced Neuronal Injury through DJ‐1‐Nrf2 Antioxidant Pathway

Cited by 16 publications

References 42 publications

The Therapeutic Potential of Metformin in Neurodegenerative Diseases

The Therapeutic Potential of Metformin in Neurodegenerative Diseases

Pharmacological activities, mechanisms of action, and safety of salidroside in the central nervous system

Implications of PI3K/AKT/PTEN Signaling on Superoxide Dismutases Expression and in the Pathogenesis of Alzheimer’s Disease

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