Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway

Arabian, Maedeh; Aboutaleb, Nahid; Soleimani, Mansoureh; Ajami, Marjan; Habibey, Rouhollah; Rezaei, Yousef; Pazoki‐Toroudi, Hamidreza

doi:10.1139/cjpp-2017-0245

Cited by 27 publications

(12 citation statements)

References 46 publications

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“…In addition, morphine protected PC12 cells against the cytotoxicity of 1-methyl-4phenylpyridinium through activating phosphatidylinositol 3-kinase (PI3K)/Akt pathway (Fan et al, 2019). Some groups demonstrated that preconditioning with morphine alleviated cerebral ischemia injury through activating the mTOR pathway (Arabian et al, 2018b) or mitochondrial KATP channels (Arabian et al, 2018a). However, repeated use of morphine will lead to various sideeffects, such as antinociceptive tolerance, dependence, and addiction.…”

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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“…TT interferes with subsequent spermatogenesis in 50% of patients and impairs borderline in another 20% (Visser & Heyns, ). Manual detorsion is successful in >80% of attempts, but reperfusion may cause a sequential chain of the pathophysiological effects, including massive intracellular Ca 2+ release, recruitment of neutrophils, acute inflammatory responses and generation of reactive oxygen species (ROS) that increases apoptotic or necrotic cell death (Ajami et al., ; Amani et al., ; Arabian et al., ; Cayan et al., ; Güneş et al., ).…”

Section: Introductionmentioning

confidence: 99%

FOXO1 targeting by capsaicin reduces tissue damage after testicular torsion

et al. 2018

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Testicular torsion-related oxidative stress causes a sequential chain of DNA damage, lipid peroxidation and cell death that leads to the derangement in the sperm functions and infertility. Capsaicin that has been applied for pain relief and cancer prevention possesses antioxidant properties which can be exploited to confer cell survival under ischaemic testis damage. Wistar male rats weighing 150-200 g were randomly divided into four groups: (i) sham group (all procedures except torsion of testis), (ii) ischaemia group (TT group), (iii) three TT groups treated with different dose of capsaicin (TT + different doses of Cap) and (iv) three control groups treated with different doses of capsaicin (100, 500 and 1000 ug/ml). Capsaicin administration significantly decreased the expression of pro-apoptotic factors and increased the expression of anti-apoptotic factors. Likewise, the expression of FOXO1 is significantly increased by higher doses of the capsaicin. Histological assessment by H&E and TUNEL method also exhibited an improved testicular morphology and decreased apoptosis in testes. These results suggested clinical potential for capsaicin in treatment of testicular torsion by targeting FOXO1 and apoptotic pathways.

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“…Seven days after cerebral ischemic injury, a passive avoidance test was conducted to assess memory performance in rats. The procedure was executed by using shuttle box according to the method described by Arabian et al (2017). Primarily, the animals were placed in the shuttle box to habituate with the surrounding.…”

Section: Passive Avoidance Testmentioning

confidence: 99%

Minocycline Improves Memory by Enhancing Hippocampal Synaptic Plasticity and Restoring Antioxidant Enzyme Activity in a Rat Model of Cerebral Ischemia-Reperfusion

Parvardeh

Sheikholeslami

Ghafghazi

et al. 2022

BCN

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Introduction: Oxidative stress plays a crucial role in the impairment of synaptic plasticity following cerebral ischemia which ultimately results in memory dysfunction. Hence, application of antioxidant agents could be beneficial in the management of memory deficit after brain ischemia. Minocycline is a tetracycline antibiotic with antioxidant effect. The main objective of this work was to assess minocycline effect on the impairment of synaptic plasticity and memory after cerebral ischemia-reperfusion in rats. Methods: Transient occlusion of common carotid arteries was used to induce ischemia-reperfusion injury in rats. Single or multiple (once daily for 7 days) doses of minocycline were administered before (pretreatment) or after (treatment) brain ischemia. Seven days after ischemia-reperfusion, passive avoidance performance, hippocampal long-term potentiation, and the activity of antioxidant enzymes were assessed. Results: The results of passive avoidance test showed that minocycline (20 and 40 mg/kg) significantly increased step-through latency while reduced the duration of staying in dark chamber in the treatment (but not pretreatment) group. In electrophysiological experiments, the rats which were treated (but not pretreated) with minocycline (40 mg/kg) showed a significant increase in the amplitude of the field excitatory postsynaptic potentials in the dentate gyrus area of hippocampus. The treatment (but not pretreatment) with minocycline (20 and 40 mg/kg) resulted in a significant increase in the activity of catalase, glutathione peroxidase, and superoxide dismutase in the hippocampus. Conclusion: It was ultimately determined that minocycline attenuates memory dysfunction after cerebral ischemia-reperfusion in rats through the improvement of hippocampal synaptic plasticity and restoration of antioxidant enzymes activity.

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Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway

Cited by 27 publications

References 46 publications

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

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

FOXO1 targeting by capsaicin reduces tissue damage after testicular torsion

Minocycline Improves Memory by Enhancing Hippocampal Synaptic Plasticity and Restoring Antioxidant Enzyme Activity in a Rat Model of Cerebral Ischemia-Reperfusion

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