Molecular Mechanism of Neuroprotective Effect of Melatonin on Morphine Addiction and Analgesic Tolerance: an Update

Su, Ling-Yan; Liu, Qianjin; Jiao, Lijin; Yao, Yong‐Gang

doi:10.1007/s12035-021-02448-0

Cited by 19 publications

(4 citation statements)

References 104 publications

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“…Morphine, a commonly used pain-relieving medication, is associated with analgesic tolerance and hyperalgesia under prolonged and repeated use [ 60 , 61 ]. The mechanisms underlying the development of morphine tolerance are diverse and complex, with the involvement of multiple signaling pathways [ 1 , 62 , 63 ]. There were many studies that reported neuronal cell death and apoptosis are involved in morphine analgesic tolerance [ 47 , 48 ].…”

Section: Discussionmentioning

confidence: 99%

S-nitrosoglutathione reductase alleviates morphine analgesic tolerance by restricting PKCα S-nitrosation

Su,

Jiao,

Liu

et al. 2024

Redox Biology

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Section: Discussionmentioning

confidence: 99%

S-nitrosoglutathione reductase alleviates morphine analgesic tolerance by restricting PKCα S-nitrosation

Su,

Jiao,

Liu

et al. 2024

Redox Biology

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“…Taking into account the disturbance of its daily production in these patients, it is not surprising that melatonin's beneficial effects were observed [54]. Although the antioxidant properties of melatonin lead to neuroprotection [55], alleviation of hypertension [56], or regulation of the activity of natural killer cells [57], this hormone has already been used only in some human diseases, and it has never been studied in MPS in light of oxidative stress prevention.…”

Section: Compounds With Antioxidant Activities and Their Effects In Mpsmentioning

confidence: 99%

Oxidative Stress in Mucopolysaccharidoses: Pharmacological Implications

et al. 2021

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Although mucopolysaccharidoses (MPS) are caused by mutations in genes coding for enzymes responsible for degradation of glycosaminoglycans, storage of these compounds is crucial but is not the only pathomechanism of these severe, inherited metabolic diseases. Among various factors and processes influencing the course of MPS, oxidative stress appears to be a major one. Oxidative imbalance, occurring in MPS and resulting in increased levels of reactive oxidative species, causes damage of various biomolecules, leading to worsening of symptoms, especially in the central nervous system (but not restricted to this system). A few therapeutic options are available for some types of MPS, including enzyme replacement therapy and hematopoietic stem cell transplantation, however, none of them are fully effective in reducing all symptoms. A possibility that molecules with antioxidative activities might be useful accompanying drugs, administered together with other therapies, is discussed in light of the potential efficacy of MPS treatment.

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“…Study has reported that the dysregulation of autophagy leads to the progression of various neurodegenerative diseases such as Alzheimer's and Parkinson's diseases [11]. Furthermore, accumulating evidences indicate that autophagy is closely related to morphine and morphine addiction [12,13]. For example, previous study have reported that morphine prompts Beclin1 expression and inhibits the interaction between Beclin1 and Bcl-2, besides, knockdown Beclin1 or knockout of autophagy-related 5 (ATG5) could both inhibit morphineinduced autophagy [14].…”

Section: Introductionmentioning

confidence: 99%

The nuclear factor E2-related factor 2 participates in morphine-induced autophagy

Huang

Feng

Deji

et al. 2022

Preprint

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Morphine is an important potent analgesic which has many side effects such as addiction. Studies have demonstrated that autophagy play an important role during morphine addiction especially in morphine withdrawal. However, the molecular basis of morphine-induced autophagy has been not fully elucidated. The nuclear factor E2-related factor 2 (NRF2) is a well-known transcription factor that plays a critical role in antioxidation and even autophagy, furthermore, previous study showed that it increased in the frontal cortex and striatum of the mice which suffering from morphine withdrawal, indicating that NRF2 may involve in morphine addiction. In the present study, we aim to clarify the role of NRF2 in morphine-induced autophagy in vitro. Our results showed morphine could significantly increase the expression of NRF2 and further induce autophagy in SH-SY5Y cells. In addition, pretreatment of NRF2 inhibitor could reverse the upregulation of NRF2 and autophagy after morphine administration, indicating NRF2 play a key role in morphine-induced autophagy. Interestingly, we found NRF2 was also regulated by autophagy because pretreated with 3-Methyladenine after morphine administration significantly increased the expression of NRF2. In conclusion, our study revealed a critical role of NRF2 in morphine-induced autophagy and the feedback effect of autophagy on NRF2.

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Molecular Mechanism of Neuroprotective Effect of Melatonin on Morphine Addiction and Analgesic Tolerance: an Update

Cited by 19 publications

References 104 publications

S-nitrosoglutathione reductase alleviates morphine analgesic tolerance by restricting PKCα S-nitrosation

S-nitrosoglutathione reductase alleviates morphine analgesic tolerance by restricting PKCα S-nitrosation

Oxidative Stress in Mucopolysaccharidoses: Pharmacological Implications

The nuclear factor E2-related factor 2 participates in morphine-induced autophagy

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