Desvenlafaxine reduces apoptosis in amygdala after myocardial infarction

Malick, Mandy; Kim, Gilbert; Barry, Mathieu; Rousseau, Guy

doi:10.1016/j.brainresbull.2014.10.012

Cited by 7 publications

(10 citation statements)

References 46 publications

(51 reference statements)

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“…An investigation about depression post-myocardial infarction also showed that DVS reduces apoptosis in limbic structures such as amygdala, brain area closely related to symptoms as anhedonia and behavioral despair observed in depression (Malick et al, 2014). These data corroborate our findings, which show a significant improvement in anhedonic-like behavior (SPT) and behavioral despair (FST) in the groups treated with DVS.…”

Section: Discussionsupporting

confidence: 91%

Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression

Sousa

Meneses

Vasconcelos

et al. 2015

Psychiatry Research

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Brain derived neurotrophic factor (BDNF) is linked to the pathophysiology of depression. We hypothesized that BDNF is one of the neurobiological pathways related to the augmentation effect of alpha-lipoic acid (ALA) when associated with antidepressants. Female mice were administered vehicle or CORT 20mg/kg during 14 days. From the 15th to 21st days the animals were divided in groups that were further administered: vehicle, desvenlafaxine (DVS) 10 or 20mg/kg, ALA 100 or 200mg/kg or the combinations of DVS10+ALA100, DVS20+ALA100, DVS10+ALA200 or DVS20+ALA200. ALA or DVS alone or in combination reversed CORT-induced increase in immobility time in the forced swimming test and decrease in sucrose preference, presenting, thus, an antidepressant-like effect. DVS10 alone reversed CORT-induced decrease in BDNF in the prefrontal cortex (PFC), hippocampus (HC) and striatum (ST). The same was observed in the HC and ST of ALA200 treated animals. The combination of DVS and ALA200 reversed CORT-induced alterations in BDNF and even, in some cases, increased the levels of this neurotrophin when compared to vehicle-treated animals in HC and ST. Taken together, these results suggest that the combination of the DVS+ALA may be valuable for treating conditions in which BDNF levels are decreased, such as depression.

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Section: Discussionsupporting

confidence: 91%

Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression

Sousa

Meneses

Vasconcelos

et al. 2015

Psychiatry Research

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“…Studies have shown that when MI occurs, myocardial apoptosis is increased, the Bax protein is upregulated and the Bcl-2 protein is downregulated in the AMI animal model and humans (15)(16)(17). Therefore, inhibiting apoptosis may be an effective method to prevent MI (18)(19)(20). In the present study, the mouse model of AMI was established to confirm that exogenous injection of Flu can effectively alleviate ischemia-induced MI, inhibit pathological changes in myocardial tissues, reduce myocardial apoptosis and increase Bcl-2 protein expression, which demonstrates that Flu can relieve ischemic-induced AMI through inhibiting myocardial apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Fluvastatin protects myocardial cells in mice with acute myocardial infarction through inhibiting RhoA/ROCK pathway

Wang

et al. 2020

Exp Ther Med

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Protective effect of fluvastatin (Flu) on myocardial cells in mice with acute myocardial infarction (AMI) and the mechanism were explored. Forty C57B/L6 mice in similar physiological status were selected and randomly divided into sham operation (Sham) group (n=10), AMI group (n=10), Flu group (n=10) and Flu + Angiotensin II (Ang II) (Ang II) group (n=10). The pathological changes in heart tissues were detected via hematoxylin and eosin (H&E) staining, and apoptosis of myocardial cells was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the expression levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were determined using relevant kits, and the expression levels of Ras homolog gene family (Rho)-associated coiled-coil protein kinase 1 (ROCK1), ROCK2, B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax) and nuclear factor-κB (NF-κB) in the infarction region were determined using Western blotting. The infarction area in mice in Flu group was significantly smaller than that in AMI group. In AMI group, the level of MDA in the serum and infarction tissues was remarkably higher than that in Sham group (P<0.05), while that of SOD significantly declined (P<0.05). The level of MDA in Flu group was obviously lower than that in AMI group (P<0.05). The expression levels of Bax, NF-κB, ROCK1 and ROCK2 were obviously higher in AMI group than those in Sham group, while they were obviously lower in Flu group than those in AMI group (P<0.05). After the Rho member A (RhoA)/ROCK pathway agonist Ang II was added, the mitigation effect of Flu on myocardial apoptosis in the infarction region in AMI mice was evidently weakened. Flu mitigates AMI-induced myocardial apoptosis in mice, and the possible mechanism is that the inflammatory and oxidative stress responses activated and mediated by RhoA/ROCK are effectively inhibited.

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“…Cellular factors, including proto-oncogenes, cytokines and Bcl-2 family members, may directly stimulate apoptotic signaling, and important membrane proteins are also associated with apoptosis, controlling apoptosis via different signals inside and outside of the cell (25). A previous study has demonstrated that certain genes, including Bax, p53 and Fas, can promote apoptosis, and other genes, such as Bcl-2 and Bax, are able to inhibit apoptosis (26). The ratio of apoptosis-inducing and apoptosis-inhibiting proteins in vivo is important for determining whether or not apoptosis will proceed; for example, if Bcl-2 protein expression is higher than that of Bax, cell survival is promoted; when Bax expression is higher than that of Bcl-2, apoptosis is accelerated (24).…”

Section: Discussionmentioning

confidence: 99%

miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression

Sun

Cai

et al. 2018

Mol Med Report

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The aim of the present study was to evaluate the functional association between the expression of miR‑483‑3p and acute myocardial infarction (AMI) in patients and in vitro. H9c2 cells were incubated in a vacuum with 5% CO2, 5% H2 and 90% N2 for 2 h, which generated the AMI model in vitro. Reverse transcription‑quantitative polymerase chain reaction was used to measure miR‑483‑3p expression, and flow cytometry analysis and ELISA analysis were used to analyze apoptosis rate via caspase‑3 and caspase‑9 activity kits. B‑cell lymphoma 2 (Bcl‑2)/Bcl‑2‑associated X protein (Bax) and transcriptionally suppressed the protein expression of insulin growth factor 1 (IGF‑1) were analyze using western blot analysis. The results demonstrated that the expression of miR‑483‑3p in patients with AMI was increased when compared with the control group. In the in vitro model, the overexpression of miR‑483‑3p promoted apoptosis, increased caspase‑3 and caspase‑9 activity levels, induced the protein expression of Bcl‑2/Bax and IGF‑1. Picropodophyllotoxin, an IGF‑1 inhibitor, was administered to cells following the overexpression of miR‑483‑3p. Administration of picropodophyllotoxin suppressed IGF‑1 protein expression, promoted apoptosis, increased caspase‑3 and caspase‑9 activity levels, and induced the protein expression of Bax/Bcl‑2. The results of the present study revealed that miR‑483‑3p may regulate AMI via the IGF‑1 signaling pathway and may support the restoration of functional performance following AMI.

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Desvenlafaxine reduces apoptosis in amygdala after myocardial infarction

Cited by 7 publications

References 46 publications

Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression

Reversal of corticosterone-induced BDNF alterations by the natural antioxidant alpha-lipoic acid alone and combined with desvenlafaxine: Emphasis on the neurotrophic hypothesis of depression

Fluvastatin protects myocardial cells in mice with acute myocardial infarction through inhibiting RhoA/ROCK pathway

miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression

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