The role of reactive oxygen species in morphine addiction of SH-SY5Y cells

Ma, Jun; Xuan, Yue; Qu, Hengyi; Zhang, Juan; Wang, Dong; Sun, Xiling; Zheng, Qin

doi:10.1016/j.lfs.2015.01.003

Cited by 37 publications

(16 citation statements)

References 39 publications

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“…It is known that HIV infection; HIV-1 gp120 protein and morphine induced ROS production lead to cell death ( Ronaldson and Bendayan, 2008 ; Ma et al, 2015 ). However, no information is available on HIV-1 gp120 and morphine induced ROS production and redox altered cell cycle arrest and neurodegeneration.…”

Section: Resultsmentioning

confidence: 99%

“…In microglia, gp120 induces oxidative stress, ROS, TNF- α , and MCP-1 production and subsequently leading to neuronal cell death ( Guo et al, 2013 ). Also, morphine was found to induce oxidative stress in in vitro as well as in vivo ( Kovacic and Cooksy, 2005 ; Ma et al, 2015 ). Studies have also shown that morphine impaired cellular function mediated by oxidative stress which affects the CNS ( Moron et al, 2009 ; Beltran-Campos et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

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HIV-1 gp120 and morphine induced oxidative stress: role in cell cycle regulation

et al. 2015

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HIV infection and illicit drugs are known to induce oxidative stress and linked with severity of viral replication, disease progression, impaired cell cycle regulation and neurodegeneration. Studies have shown that morphine accelerates HIV infection and disease progression mediated by Reactive oxygen species (ROS). Oxidative stress impact redox balance and ROS production affect cell cycle regulation. However, the role of morphine in HIV associated acceleration of oxidative stress and its link to cell cycle regulation and neurodegeneration has not been elucidated. The aim of present study is to elucidate the mechanism of oxidative stress induced glutathione synthases (GSS), super oxide dismutase (SOD), and glutathione peroxidase (GPx) impact cell cycle regulated protein cyclin-dependent kinase 1, cell division cycle 2 (CDK-1/CDC-2), cyclin B, and cell division cycle 25C (CDC-25C) influencing neuronal dysfunction by morphine co-morbidity with HIV-1 gp120. It was observed that redox imbalance inhibited the GSS, GPx and increased SOD which, subsequently inhibited CDK-1/CDC-2 whereas cyclin B and CDC-25C significantly up regulated in HIV-1 gp120 with morphine compared to either HIV-1 gp120 or morphine treated alone in human microglial cell line. These results suggest that HIV positive morphine users have increased levels of oxidative stress and effect of cell cycle machinery, which may cause the HIV infection and disease progression.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

HIV-1 gp120 and morphine induced oxidative stress: role in cell cycle regulation

et al. 2015

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“…Morphine could activate opioid receptors, and its treatment not only promoted the generation of free radicals, including reactive oxygen (ROS) or reactive nitrogen (RNS) species, but also decreased the activities of antioxidants in target cells (Skrabalova et al, 2013). Morphine could induce ROS generation in a time-and concentration-dependent manner in SH-SY5Y cells and excessive ROS subsequently affected morphine addiction through involving µ-opioid receptors (Ma et al, 2015). Systemic morphine use also led to oxidative stress in animals.…”

Section: Oxidative Stress In Morphine Addictionmentioning

confidence: 99%

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

2020

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Long-term administration of morphine for the management of chronic pain will result in tolerance to its analgesic effect and could even cause drug dependence. Numerous studies have demonstrated significant redox alteration in morphine dependence and addiction. Thioredoxin-1 (Trx-1) play important roles in controlling the cellular redox balance. In recent years, several recent studies have demonstrated that Trx-1 may be a promising novel therapeutic target for morphine addiction. In this article, we firstly review the redox alteration in morphine addiction. We also summarize the expression and the protective roles of Trx-1 in morphine dependence. We further highlight the protection of geranylgeranylacetone (GGA), a noncytotoxic pharmacological inducer of Trx-1, in morphine-induced conditioned place preference. In conclusion, Trx-1 may be very promising for clinical therapy of morphine addiction in the future.

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“…represents an important antioxidant system protecting mammalian cells against oxidative damage [50,51]. This protection is necessary as morphine treatment was reported to modulate both enzymatic and non-enzymatic antioxidant defense systems and induce oxidative stress and apoptosis under in vivo conditions [52,53].…”

Section: Plos Onementioning

confidence: 99%

Proteomic analysis of protein composition of rat hippocampus exposed to morphine for 10 days; comparison with animals after 20 days of morphine withdrawal

et al. 2020

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Opioid addiction is recognized as a chronic relapsing brain disease resulting from repeated exposure to opioid drugs. Cellular and molecular mechanisms underlying the ability of organism to return back to the physiological norm after cessation of drug supply are not fully understood. The aim of this work was to extend our previous studies of morphine-induced alteration of rat forebrain cortex protein composition to the hippocampus. Rats were exposed to morphine for 10 days and sacrificed 24 h (groups +M10 and −M10) or 20 days after the last dose of morphine (groups +M10/−M20 and −M10/−M20). The six altered proteins (�2-fold) were identified in group (+M10) when compared with group (−M10) by twodimensional fluorescence difference gel electrophoresis (2D-DIGE). The number of differentially expressed proteins was increased to thirteen after 20 days of the drug withdrawal. Noticeably, the altered level of α-synuclein, β-synuclein, α-enolase and glyceraldehyde-3phosphate dehydrogenase (GAPDH) was also determined in both (±M10) and (±M10/ −M20) samples of hippocampus. Immunoblot analysis of 2D gels by specific antibodies oriented against α/β-synucleins and GAPDH confirmed the data obtained by 2D-DIGE analysis. Label-free quantification identified nineteen differentially expressed proteins in group (+M10) when compared with group (−M10). After 20 days of morphine withdrawal (±M10/−-M20), the number of altered proteins was increased to twenty. We conclude that the morphine-induced alteration of protein composition in rat hippocampus after cessation of drug supply proceeds in a different manner when compared with the forebrain cortex. In forebrain cortex, the total number of altered proteins was decreased after 20 days without morphine, whilst in hippocampus, it was increased.

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The role of reactive oxygen species in morphine addiction of SH-SY5Y cells

Cited by 37 publications

References 39 publications

HIV-1 gp120 and morphine induced oxidative stress: role in cell cycle regulation

HIV-1 gp120 and morphine induced oxidative stress: role in cell cycle regulation

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

Proteomic analysis of protein composition of rat hippocampus exposed to morphine for 10 days; comparison with animals after 20 days of morphine withdrawal

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