ArticlePsychopharmacology2022
Therapeutic effect of Thymoquinone on behavioural response to UCMS and neuroinflammation in hippocampus and amygdala in BALB/c mice model.
Article in Psychopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Cerebral Blood Flow and Blood-Brain Barrier Water Exchange in Major Depressive Disorder: Evidence from Diffusion-Prepared Arterial Spin Labelling MRI.Brain sciences · 2025Article
- Thymoquinone regulates RSL3-induced ferroptosis in the alzheimer mouse hippocampus.Molecular biology reports · 2025Article
- A comprehensive analysis of allele-specific expression and transcriptomic profiling in pig limbic and endocrine tissues.Frontiers in molecular neuroscience · 2025Article
- MgSOFrontiers in nutrition · 2025Article
- Examining the Role of Oxytocinergic Signaling and Neuroinflammatory Markers in the Therapeutic Effects of MDMA in a Rat Model for PTSD.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Neuroinflammation in the prefrontal-amygdala-hippocampus network is associated with maladaptive avoidance behaviour.Heliyon · 2024Article
- Immune mechanisms of depression in rheumatoid arthritis.Nature reviews. Rheumatology · 2023Review
- Activation of endogenous retrovirus triggers microglial immuno-inflammation and contributes to negative emotional behaviors in mice with chronic stress.Journal of neuroinflammation · 2023Article
- Adult hippocampal neurogenesis: pharmacological mechanisms of antidepressant active ingredients in traditional Chinese medicine.Frontiers in pharmacology · 2023Review
- Emotional- and cognitive-like responses induced by social defeat stress in male mice are modulated by the BNST, amygdala, and hippocampus.Frontiers in integrative neuroscience · 2023Article
- New Insights into the Pivotal Role of the Amygdala in Inflammation-Related Depression and Anxiety Disorder.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
rationaleMajor depressive disorder is the leading cause of disability worldwide. The corticolimbic system plays a critical role in the emotional and cognitive aspects of major depressive disorder. Owing to the unsatisfactory efficacy of conventional antidepressants, there is a need to explore novel therapies.
objectivesThe current study aimed to explore the antidepressant potential of thymoquinone, a natural compound with anti-inflammatory activity, and propose its underlying mechanism of action in the unpredictable chronic mild stress (UCMS) mouse model.
methodsCoat state, forced swim test, elevated plus maze test, novelty suppressed feeding test and social interaction test were performed to quantify the behavioural shift induced by UCMS and the effect of thymoquinone and fluoxetine treatment. In addition, messenger RNA (mRNA) expression levels of inflammatory cytokines (IL-1β, IL-6 and TNF-α) and BDNF and NeuN were analysed by a quantitative real-time polymerase chain reaction in the hippocampus and amygdala of experimental and control groups.
resultsUCMS significantly deteriorated coat state. Thymoquinone reinstated the resignation behaviour and latency to feed affected by UCMS. UCMS induced an increase in inflammatory cytokines (IL-1β, IL-6 and TNF-α) in the hippocampus and amygdala, which was decreased by thymoquinone. UCMS caused an increase in BDNF and NeuN mRNA levels in the amygdala while a decrease in the hippocampus. This opposite effect on BDNF was also compensated by thymoquinone; however, thymoquinone did not significantly change Ki67 and NeuN mRNA levels in the hippocampus.
conclusionsThymoquinone restored the behavioural changes induced by UCMS. In addition, the antidepressant effect of thymoquinone is in line with changes in inflammatory parameters and changes in BDNF in the hippocampus and amygdala.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.