Therapeutic effect of Thymoquinone on behavioural response to UCMS and neuroinflammation in hippocampus and amygdala in BALB/c mice model

Nazir, Sadia; Farooq, Rai Khalid; Nasir, Sadia; Hanif, Rumeza; Javed, Aneela

doi:10.1007/s00213-021-06038-9

Cited by 12 publications

(7 citation statements)

References 68 publications

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“…In fact, stress has been shown to increase permeability and reduce the integrity of the blood-brain barrier in the AMG leading to neuroinflammation [ 32 ]. Similar to our results, increased IL-1β, IL-17, and TNF-ɑ levels in the AMG have been described in several animal models of stress, including restraint stress [ 32 ], chronic unpredictable mild stress [ 33 , 34 ] and cumulative mild stress [ 35 ]. In the latter, suppression of IL-17 effectively improved symptoms in animals exposed to cumulative mild stress early in life [ 35 ].…”

Section: Discussionsupporting

confidence: 91%

Neuroinflammation in the prefrontal-amygdala-hippocampus network is associated with maladaptive avoidance behaviour

Antunes,

Gouveia,

Kuroki

et al. 2024

Heliyon

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Section: Discussionsupporting

confidence: 91%

Neuroinflammation in the prefrontal-amygdala-hippocampus network is associated with maladaptive avoidance behaviour

Antunes,

Gouveia,

Kuroki

et al. 2024

Heliyon

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“…The possible mechanisms may involve the regulation of neurotransmitter metabolism, the influence of neuroendocrine function, synaptic plasticity, and the neural circuitry of emotion [ 97 , 98 ]. For example, chronic unpredictable stress induces both anxiety-like and depressive-like behaviors while increasing the expression of amygdala inflammatory cytokines, including IL-1β, IL-6, and TNF-α [ 99 ] ( Table 1 ). The increased cytokines can regulate the activity of amygdala neurons.…”

Section: Amygdala Neuroinflammation and Psychiatric Disordersmentioning

confidence: 99%

New Insights into the Pivotal Role of the Amygdala in Inflammation-Related Depression and Anxiety Disorder

Pan

et al. 2022

IJMS

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Depression and anxiety disorders are the two most prevalent psychiatric diseases that affect hundreds of millions of individuals worldwide. Understanding the etiology and related mechanisms is of great importance and might yield new therapeutic strategies to treat these diseases effectively. During the past decades, a growing number of studies have pointed out the importance of the stress-induced inflammatory response in the amygdala, a kernel region for processing emotional stimuli, as a potentially critical contributor to the pathophysiology of depression and anxiety disorders. In this review, we first summarized the recent progress from both animal and human studies toward understanding the causal link between stress-induced inflammation and depression and anxiety disorders, with particular emphasis on findings showing the effect of inflammation on the functional changes in neurons in the amygdala, at levels ranging from molecular signaling, cellular function, synaptic plasticity, and the neural circuit to behavior, as well as their contributions to the pathology of inflammation-related depression and anxiety disorders. Finally, we concluded by discussing some of the difficulties surrounding the current research and propose some issues worth future study in this field.

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“…Previous neuroimage studies revealed that the vulnerability of midbrain–amygdala–hippocampus/cortex functional connectivity to local inflammation was contributed to the development of anxiety and depression [ 32 – 34 ]. Microglia, the only resident immune cells in CNS, predominantly contributes to the bilaterally immuno-inflammatory response with neurons during the development of anxiety and depression [ 35 – 37 ]. Evidence from our study and others also revealed that the microglial activation played a critical role in exaggerated immuno-inflammation in CNS and that were contributed to chronic stress-induced negative emotional behaviors [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

Activation of endogenous retrovirus triggers microglial immuno-inflammation and contributes to negative emotional behaviors in mice with chronic stress

Bao

Yan

Huang

et al. 2023

J Neuroinflammation

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Background The “missing” link of complex and multifaceted interplay among endogenous retroviruses (ERVs) transcription, chronic immuno-inflammation, and the development of psychiatric disorders is still far from being completely clarified. The present study was aimed to investigate the mechanism of protective role of inhibiting ERVs on reversing microglial immuno-inflammation in basolateral amygdala (BLA) in chronic stress-induced negative emotional behaviors in mice. Methods Male C57BL/6 mice were exposed to chronic unpredictable mild stress (CUMS) for 6 w. Negative emotional behaviors were comprehensively investigated to identify the susceptible mice. Microglial morphology, ERVs transcription, intrinsic nucleic acids sensing response, and immuno-inflammation in BLA were assessed. Results Mice with chronic stress were presented as obviously depressive- and anxiety-like behaviors, and accompanied with significant microglial morphological activation, murine ERVs genes MuERV-L, MusD, and IAP transcription, cGAS–IFI16–STING pathway activation, NF-κB signaling pathway priming, as well as NLRP3 inflammasome activation in BLA. Antiretroviral therapy, pharmacological inhibition of reverse transcriptases, as well as knocking-down the ERVs transcriptional regulation gene p53 significantly inhibited microglial ERVs transcription and immuno-inflammation in BLA, as well as improved the chronic stress-induced negative emotional behaviors. Conclusions Our results provided an innovative therapeutic approach that targeting ERVs-associated microglial immuno-inflammation may be beneficial to the patients with psychotic disorders.

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Therapeutic effect of Thymoquinone on behavioural response to UCMS and neuroinflammation in hippocampus and amygdala in BALB/c mice model

Cited by 12 publications

References 68 publications

Neuroinflammation in the prefrontal-amygdala-hippocampus network is associated with maladaptive avoidance behaviour

Neuroinflammation in the prefrontal-amygdala-hippocampus network is associated with maladaptive avoidance behaviour

New Insights into the Pivotal Role of the Amygdala in Inflammation-Related Depression and Anxiety Disorder

Activation of endogenous retrovirus triggers microglial immuno-inflammation and contributes to negative emotional behaviors in mice with chronic stress

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