Rosiglitazone protects human neuroblastoma SH-SY5Y cells against acetaldehyde-induced cytotoxicity

Jung, Tae Woo; Lee, Ji Young; Shim, Wan Sub; Kang, Eun Seok; Kim, Soo‐Kyung; Ahn, Chul Woo; Lee, Hyun Chul; Soo, Bong

doi:10.1016/j.bbrc.2005.11.177

Cited by 40 publications

(36 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have demonstrated that rosiglitazone exhibits protective effects in SH-SY5Y cells, protecting cells from apoptosis by inducing the expression of antioxidant enzymes and regulating Bcl-2 and Bax expression [11, 32]. Results from our study showed that expression of Bax, a protein involved in mitochondria apoptosis signaling, was increased in MPP + group.…”

Section: Discussionsupporting

confidence: 55%

“…Additional studies have shown that peroxisome proliferator-activated receptor-gamma agonists demonstrated protective effects in a PD model [8–10]. The protective mechanisms were shown to be attributed to anti-inflammatory [9] and antioxidative [11] effects, but the specific mechanism is not clear. We hypothesize that thiazolidinedione activates expression of PGC-1 α , increases levels of PGC-1 α , and provides neuroprotective effects through the regulation of mitochondria function.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuroprotective Effect and Mechanism of Thiazolidinedione on Dopaminergic Neurons In Vivo and In Vitro in Parkinson’s Disease

Wang

Zhao

et al. 2017

PPAR Research

View full text Add to dashboard Cite

The aim of the present study was to gain insight into the neuroprotection effects and mechanism of thiazolidinedione pioglitazone in both in vitro and in vivo MPP+/MPTP induced PD models. In vivo experimental results showed that oral treatment of pioglitazone resulted in significant improvements in behavior symptoms damaged by MPTP and increase in the survival of TH positive neurons in the pioglitazone intervention groups. In addition, oral treatment of pioglitazone increased the expression of peroxisome proliferator-activated receptor-γ coactivator of 1α (PGC-1α) and increased the number of mitochondria, along with an observed improvement in mitochondrial ultrastructure. From in vitro studies, 2,4-thiazolidinedione resulted in increased levels of molecules regulated function of mitochondria, including PGC-1α, nuclear respiratory factor 1 (NRF1), NRF2, and mitochondria fusion 2 (Mfn2), and inhibited mitochondria fission 1 (Fis1). We show that protein levels of Bcl-2 and ERK were reduced in the MPP+-treated group compared with the control group. This effect was observed to be reversed upon treatment with 2,4-thiazolidinedione, as Bcl-2 and ERK expression levels were increased. We also observed that levels of the apoptotic protein Bax showed opposite changes compared to Bcl-2 and ERK levels. The results from this study confirm that pioglitazone/2,4-thiazolidinedione is able to activate PGC-1α and prevent damage of dopaminergic neurons and restore mitochondria ultrastructure through the regulation of mitochondria function.

show abstract

Section: Discussionsupporting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effect and Mechanism of Thiazolidinedione on Dopaminergic Neurons In Vivo and In Vitro in Parkinson’s Disease

Wang

Zhao

et al. 2017

PPAR Research

View full text Add to dashboard Cite

show abstract

“…The protection by rosiglitazone was attributed to the induction of the expression of anti-oxidant enzymes including SOD and catalase and by regulating the expression of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) [83]. In another study, treatment with pioglitazone was neuroprotective in rats treated with lipopolysaccharide (LPS), decreasing degeneration of dopaminergic pathways, decreasing inflammation and restoring mitochondrial function while also attenuating oxidative stress [74].…”

Section: Actions Of Pparγ In Rescuing Mitochondrial Functionmentioning

confidence: 99%

PPARγ as a therapeutic target to rescue mitochondrial function in neurological disease

Corona

Duchen

2016

Free Radical Biology and Medicine

202

127

View full text Add to dashboard Cite

There is increasing evidence for the involvement of mitochondrial dysfunction and oxidative stress in the pathogenesis of many of the major neurodegenerative and neuroinflammatory diseases, suggesting that mitochondrial and antioxidant pathways may represent potential novel therapeutic targets. Recent years have seen a rapidly growing interest in the use of therapeutic strategies that can limit the defects in, or even to restore, mitochondrial function while reducing free radical generation. The peroxisome proliferation-activated receptor gamma (PPARγ), a ligand-activated transcription factor, has a wide spectrum of biological functions, regulating mitochondrial function, mitochondrial turnover, energy metabolism, antioxidant defence and redox balance, immune responses and fatty acid oxidation. In this review, we explore the evidence for potential beneficial effects of PPARγ agonists in a number of neurological disorders, including Parkinson’s disease, Alzheimer’s disease, Amyotrophic lateral sclerosis and Huntington’s disease, ischaemia, autoimmune encephalomyelitis and neuropathic pain. We discuss the mechanisms underlying those beneficial effects in particular in relation to mitochondrial function, antioxidant defence, cell death and inflammation, and suggest that the PPARγ agonists show significant promise as therapeutic agents in otherwise intractable neurological disease.

show abstract

“…PPAR γ agonists have also been tested in neuronal cells treated with acetaldehyde, a toxin that mimics Parkinson disease (PD) neurodegeneration [40]. Acetaldehyde is an inhibitor of mitochondrial function and induced oxidative stress and apoptosis in neuronal cells [41].…”

Section: Pparγ Activation Prevents Neurodegenerationmentioning

confidence: 99%

Role of PPARγin the Differentiation and Function of Neurons

2014

View full text Add to dashboard Cite

Neuronal processes (neurites and axons) have an important role in brain cells communication and, generally, they are damaged in neurodegenerative diseases. Recent evidence has showed that the activation of PPARγ pathway promoted neuronal differentiation and axon polarity. In addition, activation of PPARγ using thiazolidinediones (TZDs) prevented neurodegeneration by reducing neuronal death, improving mitochondrial function, and decreasing neuroinflammation in neuropathic pain. In this review, we will discuss important evidence that supports a possible role of PPARγ in neuronal development, improvement of neuronal health, and pain signaling. Therefore, activation of PPARγ is a potential target with therapeutic applications against neurodegenerative disorders, brain injury, and pain regulation.

show abstract

Rosiglitazone protects human neuroblastoma SH-SY5Y cells against acetaldehyde-induced cytotoxicity

Cited by 40 publications

References 24 publications

Neuroprotective Effect and Mechanism of Thiazolidinedione on Dopaminergic Neurons In Vivo and In Vitro in Parkinson’s Disease

Neuroprotective Effect and Mechanism of Thiazolidinedione on Dopaminergic Neurons In Vivo and In Vitro in Parkinson’s Disease

PPARγ as a therapeutic target to rescue mitochondrial function in neurological disease

Role of PPARγin the Differentiation and Function of Neurons

Contact Info

Product

Resources

About