Low concentration of morphine protects against cell death, oxidative stress and calcium accumulation by nicotine in PC12 cells

Amini, Keyvan; Zhaleh, H; Tahvilian, Reza; Farnia, Vahid

doi:10.4149/bll_2019_042

Cited by 4 publications

(4 citation statements)

References 26 publications

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“…An increasing number of studies have clarified that morphine could display beneficial protection. Morphine at low concentrations promoted cell proliferation and suppressed nicotine-induced cytotoxicity and cell death in PC12 cells (Amini et al, 2019). Low-dose morphine played a neuroprotective role in cellular and animal models of Parkinson's disease through inhibiting oxidative stress and endoplasmic reticulum stress, promoting autophagy activation, and improving mitochondrial function (Wang et al, 2018).…”

Section: Introductionmentioning

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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Section: Introductionmentioning

confidence: 99%

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

2020

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“…At low concentration, morphine is found to have promoted cell proliferation and suppressed nicotine-induced cell death in PC12 cells [15,16]. It was also demonstrated to have neuroprotective roles in Parkinson's disease models by the improvement of mitochondrial function via the inhibition of ROS production [16,17].…”

Section: Discussionmentioning

confidence: 99%

Investigation of Reactive Oxygen Species production in Human Hepatocytes

Agbedanu¹,

Puga²,

Schafer³

et al. 2022

JGPHD

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1. Aim/Background: Reactive oxygen species (ROS) have been identified as compounds responsible for producing cellular damage. The purpose of this research is to examine if there is production of reactive oxygen species through free radical intermediates within human hepatocytes treated with morphine, bilirubin, or furosemide. The investigation examines the early stages of biotransformation by measuring the levels of reactive oxygen species produced inside of the treated hepatocytes within the first and second hours of treatment. The experiment was designed upon a case of a jaundiced (elevated bilirubin) infant who received morphine and furosemide and later died through unknown mechanisms. The experiment looks to examine if these drug compounds could contribute to cellular damage. This can help to further understand the potential interactions and complications of free radical intermediates produced during the phases of biotransformation. 2. Method: Previously cultured human hepatocytes were washed by centrifugation and re-suspended in 1x supplemental buffer to a concentration of 1x106 cells/mL and seeded in a dark clear bottom 96-well microplate at 100,000 stained cells/well. The cells were treated with either furosemide, morphine, bilirubin, a Tert-Butyl hydro peroxide (TBHP) positive control, or left as a background. Reactive oxygen generated in the presence of these agents were quantified by fluorescence excitation/emission measurement at 495nm/529nm. Fluorescence was measured at one and two hours. ROS generated convert 2',7'-dichlorodihydrofluorescein diacetate to 2',7'-dichlorodihydrofluorescein within the cells, which fluoresces. The fluorescence intensity detected is equivalent to the level of ROS generated. Wells that were untreated were used as blanks and subtracted from background and TBPH. 3. Results: Furosemide and Morphine did not produce statistically significant levels of ROS (p >0.05) above the background in both hours 1 and 2 of biotransformation and ROS measurement (Figure 1). Although Bilirubin did not produce statistically significant (p >0.05) levels of ROS above the background (Figure 2) during the first hour, it did produce statistically significant levels in the second hour of biotransformation. Each compound’s level of ROS was reduced during the second hour, signaling the removal of intermediate ROS metabolites (Figure 2). The production of ROS in each compound signifies that there is biotransformation to an intermediate that produces ROS. 4. Conclusion: The production of ROS above the background by each of the compounds shows there is an intermediate free radical compound that is produced during the biotransformation of each compound [21]. In this study, although furosemide and morphine did not produce statistically significant levels of ROS in both hours of biotransformation, bilirubin did produce significant levels of ROS in the second hour of biotransformation. This finding is in line with previous studies that shows morphine to offer protective effects against ROS production [16, 17]; and bilirubin demonstrating deleterious production of ROS at high doses [18]. Further work must be done to examine the correlation between the levels of ROS and extent of hepatocellular damage.

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“…However, we are cognizant that in recent years, many studies have shown that morphine can also exert neuroprotective effects through various mechanisms [ 28 ]. The main mechanisms include reducing intracellular Ca 2+ overload, reducing cell oxidative damage, activating autophagy, and inhibiting intracellular toxic protein production to promote neuronal regeneration and differentiation [ 29 , 30 , 31 , 32 ]. At the same time, researchers have applied very low doses of morphine to very preterm infants, which has effectively improved the neurodevelopmental status of the infants [ 33 ].…”

Section: Isoquinoline Alkaloids With Neuroprotective Effectsmentioning

confidence: 99%

Research Progress on Neuroprotective Effects of Isoquinoline Alkaloids

Dong

et al. 2023

Molecules

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Neuronal injury and apoptosis are important causes of the occurrence and development of many neurodegenerative diseases, such as cerebral ischemia, Alzheimer’s disease, and Parkinson’s disease. Although the detailed mechanism of some diseases is unknown, the loss of neurons in the brain is still the main pathological feature. By exerting the neuroprotective effects of drugs, it is of great significance to alleviate the symptoms and improve the prognosis of these diseases. Isoquinoline alkaloids are important active ingredients in many traditional Chinese medicines. These substances have a wide range of pharmacological effects and significant activity. Although some studies have suggested that isoquinoline alkaloids may have pharmacological activities for treating neurodegenerative diseases, there is currently a lack of a comprehensive summary regarding their mechanisms and characteristics in neuroprotection. This paper provides a comprehensive review of the active components found in isoquinoline alkaloids that have neuroprotective effects. It thoroughly explains the various mechanisms behind the neuroprotective effects of isoquinoline alkaloids and summarizes their common characteristics. This information can serve as a reference for further research on the neuroprotective effects of isoquinoline alkaloids.

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Low concentration of morphine protects against cell death, oxidative stress and calcium accumulation by nicotine in PC12 cells

Cited by 4 publications

References 26 publications

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

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

Investigation of Reactive Oxygen Species production in Human Hepatocytes

Research Progress on Neuroprotective Effects of Isoquinoline Alkaloids

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