Morphine Addiction and Oxidative Stress: The Potential Effects of Thioredoxin-1

Zeng, Xiansi; Wang, Zhan-Qi; Jia, Jinjing

doi:10.3389/fphar.2020.00082

Cited by 44 publications

(33 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2 ). The protection of Sal at 50 μM was better than that of Geranylgeranylacetone (GGA), which is a Trx inducer and a protective agent against MPP + 12 , 24 . However, the protective effect of Sal was inhibited by co-treated with 2-[(1-Methylpropyl) dithio]-1H-imidazole (PX-12), a Trx1 inhibitor 25 , 26 .…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Thioredoxin-1 mediates neuroprotection of Schisanhenol against MPP+-induced apoptosis via suppression of ASK1-P38-NF-κB pathway in SH-SY5Y cells

Yang

Jiao

et al. 2021

Sci Rep

View full text Add to dashboard Cite

Oxidative stress-induced dopaminergic neuronal loss and apoptosis play a crucial role in the pathogenesis of Parkinson’s disease (PD), and as a vital antioxidant protein, thioredoxin (Trx) exerts neuroprotection against PD. In this study, we investigated the effect of Schisanhenol (Sal), an active component from a traditional Chinese herb Schisandra rubriflora (Franch.), on MPP+-induced apoptosis and its association with thioredoxin-1 (Trx1) in SH-SY5Y cells. The protein levels of Trx1 and apoptosis-related proteins were detected by Western blot, the expression of Trx1 mRNA by real time qPCR, and apoptosis was detected by fluorescence microscopy and flow cytometry. Pretreatment with Sal (1 µM, 10 µM, and 50 µM) dose-dependently ameliorated MPP+-induced neuronal injury, confirmed by the improvement of the viability and morphological changes. Sal decreased the apoptosis rate of cells, suppressed the production of DNA ladder and sub-G1 peak, inhibited the Caspase-3 activity and the expression of apoptosis-related proteins. Sal enhanced the expression of Trx1 both in the protein and mRNA levels. However, the Trx1 inhibitor PX-12 suppressed the protective effects of Sal. In addition, Sal inhibited NF-κB translocation and activation. These results suggest that Sal has a protective effect against MPP+-induced apoptosis in SH-SY5Y cells via up-regulation of Trx1 expression and suppression of ASK1-P38-NF-κB pathway.

show abstract

Section: Resultsmentioning

confidence: 99%

“…These results indicate that Trx1 was involved in the protective effect of Sal against MPP + -induced apoptosis in SH-SY5Y cells. GGA is a Trx1 inducer and has a protective agent against MPP + 12 , 24 . In the present study, the protective effect of Sal (50 μM) was similar to that of GGA.…”

Section: Discussionmentioning

confidence: 99%

Thioredoxin-1 mediates neuroprotection of Schisanhenol against MPP+-induced apoptosis via suppression of ASK1-P38-NF-κB pathway in SH-SY5Y cells

Yang

Jiao

et al. 2021

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Trx couples with Prx to scavenge ROS, such as directly converting H 2 O 2 to H 2 O (Granger and Kvietys, 2015). Our previous studies demonstrated that Trx exerted protective effects in oxidative stress, morphine and methamphetamine addiction, autoimmune disease, cerebral ischemic damage and cancers (Chen et al., 2014; Zeng, Zhou, et al., 2014; Zeng et al., 2015; Jia et al., 2019; L. Yang et al., 2020; Zeng et al., 2020). Trx was reported to improve the learning and memory ability of Parkinsonism mice (X.…”

Section: Trxs In Admentioning

confidence: 99%

The Potential Roles of Redox Enzymes in Alzheimer’s Disease: Focus on Thioredoxin

Jia

Zeng

et al. 2021

ASN Neuro

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is the most common neurodegenerative diseases. Increasing studies have demonstrated the critical importance for redox proteins mediating neuronal protection in models of AD. This review briefly describes some of the risk factors contributing to AD, specifically highlighting the important roles of oxidative stress in the pathology of AD. Then this article concisely introduces the dysregulation and functions of two main redox enzymes, peroxiredoxins and glutaredoxins, in AD models. This review emphasizes the neuroprotective role of the third redox enzyme thioredoxin (Trx), an important multifunctional protein regulating cellular redox status. This commentary not only summarizes the alterations of Trx expression in AD patients and models, but also reviews the potential effects and mechanisms of Trx, Trx-related molecules and Trx-inducing compounds against AD. In conclusion, Trx has a potential neuroprotection in AD and may be very promising for clinical therapy of AD in the future.

show abstract

“…Our results have shown that NR1 can induce the expression of Trx-1. Trx-1 played a vital role in various diseases, including ischemic stroke ( Qi et al, 2015 ), morphine addiction ( Zeng et al, 2020 ), and Parkinson’s disease ( Zeng et al, 2014 ). Besides, Wang et al proved that NR1 alleviated ROS which was induced by high glucose present in RSC96 cells ( Wang et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Notoginsenoside R1 Protects Against the Acrylamide-Induced Neurotoxicity via Upregulating Trx-1-Mediated ITGAV Expression: Involvement of Autophagy

Wang

Thomas

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

Acrylamide (ACR) is a common chemical used in various industries and it said to have chronic neurotoxic effects. It is produced during tobacco smoking and is also generated in high-starch foods during heat processing. Notoginsenoside R1 (NR1) is a traditional Chinese medicine, which is used to improve the blood circulation and clotting. The objective of this study was to investigate the mechanism of ACR-triggered neurotoxicity and to identify the protective role of NR1 by upregulating thioredoxin-1 (Trx-1). Our results have shown that NR1 could block the spatial and cognitive impairment caused by ACR administration. Bioinformatics analysis revealed that Trx-1 regulated autophagy via Integrin alpha V (ITGAV). NR1 could resist the ACR-induced neurotoxicity by upregulating thioredoxin-1 in PC12 cells and mice. The autophagy-related proteins like autophagy-related gene (ATG) 4B, Cathepsin D, LC3 II, lysosomal-associated membrane protein 2a (LAMP2a), and ITGAV were restored to normal levels by NR1 treatment in both PC12 cells and mice. Besides, we also found that overexpression of Trx-1 resisted ACR-induced autophagy in PC12 cells and downregulation of Trx-1 triggered autophagy induced by ACR in PC12 cells. Therefore, it could be concluded that Trx-1 was involved in the autophagy pathway. Besides, we also found that ITGAV was an intermediate node linking Trx-1 and the autophagy pathway.

show abstract

Morphine Addiction and Oxidative Stress: The Potential Effects of Thioredoxin-1

Cited by 44 publications

References 64 publications

Thioredoxin-1 mediates neuroprotection of Schisanhenol against MPP+-induced apoptosis via suppression of ASK1-P38-NF-κB pathway in SH-SY5Y cells

Thioredoxin-1 mediates neuroprotection of Schisanhenol against MPP+-induced apoptosis via suppression of ASK1-P38-NF-κB pathway in SH-SY5Y cells

The Potential Roles of Redox Enzymes in Alzheimer’s Disease: Focus on Thioredoxin

Notoginsenoside R1 Protects Against the Acrylamide-Induced Neurotoxicity via Upregulating Trx-1-Mediated ITGAV Expression: Involvement of Autophagy

Contact Info

Product

Resources

About