BDNF prevents central oxidative damage in a chronic unpredictable mild stress model: The possible role of PRDX-1 in anhedonic behavior

Scotton, Ellen; Colombo, Rafael; Reis, Jéssica C.; Possebon, Gabriela M.P.; Hizo, Gabriel Henrique; Valiati, Fernanda Endler; Géa, Luíza Paul; Bristot, Giovana; Salvador, Mirian; Silva, Tuani M.; Guerra, Alessandra E.; Lopes, Tiago Falcón; Rosa, Adriane Ribeiro; Kunz, Maurício

doi:10.1016/j.bbr.2019.112245

Cited by 22 publications

(20 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although there are various investigated brain regions responsible for mood regulation [32,33], the majority of studies in the field of behavioral alterations are focused on the hippocampus [34,35]. It is worth noticing that increased oxidative damage in all specific brain regions responsible for mood regulation correlates with mood disorders [36,37].…”

Section: Discussionmentioning

confidence: 99%

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

et al. 2019

View full text Add to dashboard Cite

Since cisplatin therapy is usually accompanied with numerous toxicities, including neurotoxicity, that involve tissue oxidative damage, the aim of this study was to evaluate the possible protective effect of N-acetylcysteine (NAC) on the anxiogenic response to cisplatin (CIS). Thirty-two male Wistar albino rats divided into four groups (control, cisplatin, NAC, and CIS + NAC). All treatments were delivered intraperitoneally. On day one, the control and cisplatin groups received saline while the NAC and CIS + NAC groups were administered with NAC (500 mg/kg). On the fifth day, the control group received saline while the CIS group was treated with cisplatin (7.5 mg/kg), the NAC group again received NAC (500 mg/kg), and the CIS + NAC group was simultaneously treated with cisplatin and NAC (7.5 and 500 mg/kg, respectively). Behavioral testing, performed on the tenth day in the open field (OF) and elevated plus maze (EPM) tests, revealed the anxiogenic effect of cisplatin that was significantly attenuated by NAC. The hippocampal sections evaluation showed increased oxidative stress (increased lipid peroxidation and decline in antioxidant enzymes activity) and proapoptotic action (predominantly by diminished antiapoptotic gene expression) following a single dose of cisplatin. NAC supplementation along with cisplatin administration reversed the prooxidative and proapoptotic effects of cisplatin. In conclusion, the results obtained in this study confirmed that antioxidant supplementation with NAC may attenuate the cisplatin-induced anxiety. The mechanism of anxiolytic effect achieved by NAC may include the decline in oxidative damage that down regulates increased apoptosis and reverses the anxiogenic action of cisplatin.

show abstract

Section: Discussionmentioning

confidence: 99%

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

et al. 2019

View full text Add to dashboard Cite

show abstract

“…From the study results, five studies were showing a significant reduction in BDNF levels in stressed mice compared to controls, and one study showed an increase in BDNF in stressed mice, namely Scotton et al (2019) (p = 0.001).…”

Section: Resultsmentioning

confidence: 99%

“…The duration of treatment in each study was almost the same, namely for two weeks except in Scotton et al (2019) in mice with CUMS for six weeks, and in the Ghooshchi and Jahromi (2018) study, there was an EX (exercise) group who received 1-2 sessions of recording to show acute conditions and two weeks for chronic. The duration of the intervention showed the duration of the stressor given to the mice, and almost all studies lasted two weeks which could indicate chronic conditions.…”

Section: Resultsmentioning

confidence: 99%

Expression of Brain-Derived Neurotrophic Factor in the Brain of Depressed Mice: Systematic Literature Review

As¹,

Veterini²,

Algristian³

et al. 2021

Qanun Medika

View full text Add to dashboard Cite

Introduction: Chronic stress exposure plays a role as a risk factor for depression. In chronic stress, there is prunning of nerve cell dendrites so that depression becomes irreversible. Depression is caused by low serotonin (5-HT2) neurotransmitters in the postsynaptic cleft. Recent findings in experimental animals indicate that serotonergic preparations are required to increase serotonin levels in the synapse opening, thereby triggering the formation of new dendrites to make depression reversible. The different results when these preparations create resistance in cases of chronic depression and actually increase the risk of uncomfortable and even fatal side effects with long-term use.Methods: This Systematic Literature Review uses the PubMed and Google Scholar databases for the period 2015-2020. A total of 322 articles at the beginning of identification and those that met the inclusion criteria in this study were six articles.Results: The results of data extraction showed that the depression condition caused by various stressors resulted in BDNF levels in the hippocampus decreased significantly by p≤0.005.Conclusion: Based on the literature study, it was concluded that in depressive conditions, BDNF levels in the brain decreased.

show abstract

“…A previous study indicated that Prx1 appeared to act as a sensitive biomarker to ROS (e.g., H 2 O 2 ) and represented an initial response to stress to maintain redox homeostasis, preventing oxidative damage to lipids and proteins (Scotton et al, 2020). In addition, Prx1 negatively regulated TLR4 signaling for NF-kB activation by inhibiting TRAF6 ubiquitin-ligase activity (Min et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Danhong Injection Protects Hemorrhagic Brain by Increasing Peroxiredoxin 1 in Aged Rats

Wang

Sun

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

Intracerebral hemorrhage (ICH) is a severe cerebrovascular disease with a high incidence, mortality and disability rate. Danhong injection (DHI) is beneficial for ischemic stroke, but is prohibited for ICH due to risk of bleeding. The present study aims to explore the potential therapeutic time window and molecular mechanism of DHI in a collagenase-induced ICH model in aged rats. DHI administration after ICH could significantly improve body weight and neurological deficits, and reduce the hematoma volume and brain water content when compared to the vehicle control. Furthermore, the protective effect of DHI administration on days 1-3 after ICH was superior to those on days 3-5 or 7-9 after ICH. DHI remarkably increased the Peroxiredoxin 1 (Prx1) expression in astrocytes and reduced the expression of inflammatory factors tumor necrosis factor-a (TNF-a) and interleukin-b (IL-1b) after ICH. The immediate treatment of Prx1 inhibiter chelerythrine (Che) after ICH abolished the protective effect of DHI. Furthermore, the Che treatment reduced the expression of Prx1 in astrocytes, but increased the expression of TNF-a and IL-1b after ICH. DHI treatment could not reverse these changes. Therefore, the earlier DHI is administered, the better the neuroprotective effect. DHI exerts antioxidative and antiinflammatory function by increasing Prx1 in astrocytes. These present results may change the established understanding of DHI, and reveal a novel treatment approach for ICH.

show abstract

BDNF prevents central oxidative damage in a chronic unpredictable mild stress model: The possible role of PRDX-1 in anhedonic behavior

Cited by 22 publications

References 70 publications

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

Expression of Brain-Derived Neurotrophic Factor in the Brain of Depressed Mice: Systematic Literature Review

Danhong Injection Protects Hemorrhagic Brain by Increasing Peroxiredoxin 1 in Aged Rats

Contact Info

Product

Resources

About