Maternal Oral Consumption of Morphine Increases Bax/Bcl-2 Ratio and Caspase 3 Activity During Early Neural System Development in Rat Embryos

Nasiraei-Moghadam, Shiva; Kazeminezhad, Behrang; Dargahi, Leila; Ahmadiani, Abolhassan

doi:10.1007/s12031-009-9312-6

Cited by 41 publications

(36 citation statements)

References 64 publications

(66 reference statements)

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“…Pharmacology manifested by the increase in caspase-3, Bax proteins, and decrease in Bcl-2 proteins in the brain [6][7][8]. In addition, studies suggest that mitochondria dysfunction and internal apoptotic pathways can play a prominent role in mediating opioid-induced neurotoxicity [8,9].…”

Section: Fundamental and Clinicalmentioning

confidence: 99%

The effect of various morphine weaning regimens on the sequelae of opioid tolerance involving physical dependency, anxiety and hippocampus cell neurodegeneration in rats

Motaghinejad

Karimian

Motaghinejad

et al. 2015

Fundamemntal Clinical Pharma

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Chronic consumption of morphine induces physical dependency, anxiety, and neurodegeneration. In this study, morphine on its own has been used for the management of morphine-induced dependency, oxidative stress, and apoptosis. Forty-eight male rats were randomly divided into six groups. Rats in groups 1-5 were made morphine dependent by an increasing manner of morphine for 7 days (15-45 mg/kg). For the next 14 days, morphine was administered using the following regimen: (i) once daily 45 mg/kg (positive controls), (ii) the same dose at additional intervals (6 h longer than the previous intervals each time), (iii) 45 mg/kg of morphine at irregular intervals like of 12, 24, 36 h, (iv) decreasing dose once daily (every time 2.5 mg/kg less than the former dosage). Group 5 received 45 mg/kg of morphine and 10 mg/kg of SOD mimetic agent (M40401) injection per day. Group 6 (negative control) received saline solution only. On day 22, all animals received naloxone (3 mg/kg) and their Total Withdrawal Index (TWI) and blood cortisol levels were measured. After drug treatment, hippocampus cells were isolated, and oxidative, antioxidative, and apoptotic factors were evaluated. Various regimens of morphine reduced TWI, cortisol levels, Bax activity, caspase-3, caspase-9, TNF-α, and IL-1β and lipid peroxidation. In all treatment groups, GSH level, superoxide dismutase, glutathione peroxidase, and Bcl-2 activity were significantly increased. Furthermore, SOD mimetic agent c diminished morphine effect on SOD activity. Thus, varying the dosage regimen of morphine can reduce the severity of morphine-induced dependency and neurodegeneration.

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Section: Fundamental and Clinicalmentioning

confidence: 99%

The effect of various morphine weaning regimens on the sequelae of opioid tolerance involving physical dependency, anxiety and hippocampus cell neurodegeneration in rats

Motaghinejad

Karimian

Motaghinejad

et al. 2015

Fundamemntal Clinical Pharma

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“…The slides were then counterstained with hematoxylin, dehydrated using graded alcohols and xylene, and observed at 400 amplification times of light microscopy. Brown granules represented positive staining, and the number of positive cells in five randomly chosen fields was counted (Nasiraei-Moghadam et al, 2010).…”

Section: Detection Of Bcl-2 and Bax Expressionmentioning

confidence: 99%

Protective effect of Danhong injection on cerebral ischemia–reperfusion injury in rats

Wan

et al. 2012

Journal of Ethnopharmacology

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“…This is essential when dealing with drug exposure, as the effects observed in mammalian embryos might be due to the susceptibility of the mother and not the embryo per se . The study of the morphine direct effects in the embryos will provide a better understanding on the molecular mechanisms that underlie the physical and neurobehavioral defects shown in fetuses and offspring after maternal morphine consumption (Nasiraei-Moghadam et al, 2010). Also, the endogenous opioid system has been characterized in the zebrafish, and contains a mu opioid receptor (zfMOR), two DOR duplicates (zfDOR1 and zfDOR2), a kappa opioid receptor (zfKOR) and an opioid receptor like (zfORL) gene (Barrallo et al, 2000; Rodriguez et al, 2000; Alvarez et al, 2006; Pinal-Seoane et al, 2006).…”

Section: Zebrafish As a Model To Study The Relationship Between Mir-1mentioning

confidence: 99%

Morphine and microRNA Activity: Is There a Relation with Addiction?

Rodrı́guez¹

2012

Front. Gene.

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When we talk about drug addiction, we are really dealing with an extremely complex system in which there still remain many unknowns and where many empty spaces or missing links are still present. Recent studies have identified changes in the expression profiles of several specific miRNAs which affect the interactions between these molecules and their targets in various illnesses, including addiction, and which may serve as valuable targets for more efficient therapies. In this review, we summarize results which clearly demonstrate that several morphine-related miRNAs have roles in the mechanisms that define addiction. In this regard, morphine has been shown to have an important role in the regulation of different miRNAs, such as miR-let-7 [which works as a mediator of the movement of the mu opioid receptor (MOR) mRNA into P-bodies, leading to translational repression], miR-23b (involved in linking MOR expression and morphine treatment at the post-transcriptional level), and miR-190 (a key post-transcriptional repressor of neurogenic differentiation, NeuroD). Fentanyl increases NeuroD levels by reducing the amount of miR-190, but morphine does not affect the levels of NeuroD. We also discuss the relationship between morphine, miRNAs, and the immune system, based on the discovery that morphine treatment of monocytes led to a decrease in several anti-HIV miRNAs (mir-28, 125b, 150, and 382). This review is centered on miR-133b and its possible involvement in addiction through the effects of morphine. We establish the importance of miR-133b as a regulatory factor by summarizing its activity in different pathological processes, especially cancer. Using the zebrafish as a research model, we discuss the relationship between mir-133b, the dopaminergic system, and morphine, considering: (1) that morphine modulates the expression of miR-133b and of its target transcript Pitx3, (2) the role of the zebrafish mu opioid receptor (zfMOR) in morphine-induced regulation of miR-133b, which depends on ERK1/2, (3) that morphine regulates miR-133b in hippocampal neurons, and (4) the role of delta opioid receptors in morphine-induced regulation of miR-133b. We conclude that the control of miR-133b levels may be a mechanism for the development of addiction to morphine, or other drugs of abuse that increase dopaminergic levels in the extracellular space. These results show that miR-133b is a possible new target for the design of new treatments against addictive disorders.

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Maternal Oral Consumption of Morphine Increases Bax/Bcl-2 Ratio and Caspase 3 Activity During Early Neural System Development in Rat Embryos

Cited by 41 publications

References 64 publications

The effect of various morphine weaning regimens on the sequelae of opioid tolerance involving physical dependency, anxiety and hippocampus cell neurodegeneration in rats

The effect of various morphine weaning regimens on the sequelae of opioid tolerance involving physical dependency, anxiety and hippocampus cell neurodegeneration in rats

Protective effect of Danhong injection on cerebral ischemia–reperfusion injury in rats

Morphine and microRNA Activity: Is There a Relation with Addiction?

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