Nrf2 Alleviates Cognitive Dysfunction and Brain Inflammatory Injury via Mediating Wfs1 in Rats with Depression-Like Behaviors

Huang, Xiao; Qu, Qing; Ren, Dongmei

doi:10.1007/s10753-021-01554-4

Cited by 3 publications

(2 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The studies included here were based on different animal depression paradigms, with many studies using stress-induced DLB, mostly elicited by LPS [ 40 , 43 , 51 , 53 , 58 , 59 , 63 , 65 , 67 , 73 , 75 , 79 , 85 , 88 , 95 , 105 , 106 , 125 ], or through corticosterone or cortisol [ 44 , 46 , 80 , 87 , 98 ], while other studies used chronic unpredictable mild stress [ 61 , 72 , 76 , 83 , 93 , 96 , 97 , 99 , 100 , 101 , 106 , 108 , 111 , 122 , 124 ] or social defeat stress [ 50 , 52 , 88 , 102 , 107 , 120 ]. Two studies used tumour-related depression models [ 71 , 91 ], while just one study each used post-ovariectomised depression [ 121 ], pentylenetetrazol-induced seizures [ 116 ], maternal separation [ <...…”

Section: Discussionmentioning

confidence: 99%

The Nrf2 Pathway in Depressive Disorders: A Systematic Review of Animal and Human Studies

et al. 2023

View full text Add to dashboard Cite

There is increasing interest in the involvement of antioxidative systems in protecting from depression. Among these, Nrf2 occupies a central place. We aimed to review the role of Nrf2 in depression. For this reason, we conducted a PubMed search using as search strategy (psychiatr*[ti] OR schizo*[ti] OR psychot*[ti] OR psychos*[ti] OR depress*[ti] OR MDD[ti] OR BD[ti] OR bipolar[ti] OR Anxiety[ti] OR antidepress*[ti] OR panic[ti] OR obsess*[ti] OR compulsio*[ti] OR “mood disord*”[ti] OR phobi*[ti] OR agoraphob*[ti] OR anorex*[ti] OR anorect*[ti] OR bulimi*[ti] OR “eating disorder*”[ti] OR neurodevelopm*[ti] OR retardation[ti] OR autism[ti] OR autistic[ti] OR ASM[ti] OR adhd[ti] OR “attention-deficit”[ti]) AND nrf2, which on the 9th of March produced 208 results of which 89 were eligible for our purposes. Eligible articles were studies reporting data of Nrf2 manipulations or content by any treatment in human patients or animals with any animal model of depression. Most studies were on mice only (N = 58), 20 on rats only, and three on both rats and mice. There were two studies on cell lines (in vitro) and one each on nematodes and fish. Only four studies were conducted in humans, one of which was post mortem. Most studies were conducted on male animals; however, human studies were carried out on both men and women. The results indicate that Nrf2 is lower in depression and that antidepressant methods (drugs or other methods) increase it. Antioxidant systems and plasticity-promoting molecules, such as those in the Nrf2–HO-1, BDNF–TrkB, and cyclic AMP–CREB pathways, could protect from depression, while glycogen synthase kinase-3β and nuclear factor κB oppose these actions, thus increasing depressive-like behaviours. Since Nrf2 is also endowed with tumorigenic and atherogenic potential, the balance between benefits and harms must be taken into account in designing novel drugs aiming at increasing the intracellular content of Nrf2.

show abstract

Section: Discussionmentioning

confidence: 99%

The Nrf2 Pathway in Depressive Disorders: A Systematic Review of Animal and Human Studies

et al. 2023

View full text Add to dashboard Cite

show abstract

“…In the meantime, Huang et al discovered that miR-17-5p bound to target mRNAs to a lesser extent than Nrf2 (nuclear factor erythroid-2-related factor 2) in the hippocampus of CUMS rats, and overexpression of Nrf2 competitively inhibited miR-17-5p expression, thereby promoting transcription of miR-17-5p-targeted Wfs1 (Wolfram Syndrome Protein 1) and alleviating cognitive dysfunction and brain inflammation mechanisms to achieve antidepressant effects [46]. In the hippocampal dentate gyrus (DG) of the depressed rat model, the expression of miR-26a-3p, miR-211-5p, and miR-204-5p was downregulated, involving activation of PTEN (phosphatase and tensin homolog)/PI3K (phosphatidylinositol 3-kinase)/Akt (protein kinase B) signaling pathway, Dyrk1A (dualspecificity tyrosine-(Y)-phosphorylation regulated kinase 1A)/STAT3 (signal transducer and activator of transcription 3) signaling pathway as well as aberrant expression of regulator of G-protein signaling 12 (RGS12), and overexpression of these miRNAs contribute to the inhibition of neuroinflammation, neuronal apoptosis, and depression-like behavior [47][48][49]. Thus, they are expected to be potential targets for the treatment of depression.…”

Section: Rat Modelmentioning

confidence: 99%

Research progress of miRNA in different depression model samples

Zhang¹

2022

AETR

View full text Add to dashboard Cite

Depression is a mood disorder characterized by prolonged depressed mood, lack of interest and pleasure, and low self-assessment. The miRNAs, as single-stranded non-coding RNA molecules that can participate in post-transcriptional regulation of gene expression, regulate physiological processes by degrading mRNAs or inhibiting the translation of their target genes to achieve gene silencing. Numerous studies have revealed an in-depth understanding of depression-related miRNA changes and the role they play in the pathogenesis of depression, and miRNAs have received widespread attention as therapeutic targets. This review summarizes the expression of miRNAs in different depression samples (patients, rats, and mice) and the corresponding regulatory pathways. The analysis revealed the existence of miRNAs with consistent expression trends in different samples, and the discovery of these miRNAs provides new insights into their use as therapeutic targets in depression.

show abstract

Associations of Dietary Vitamin A and Beta-Carotene Intake With Depression. A Meta-Analysis of Observational Studies

2022

View full text Add to dashboard Cite

ObjectiveTo clarify the associations of dietary vitamin A and beta-carotene intake with depression based on a meta-analysis of observational studies.MethodsAn extensive literature search on February 2022 (PubMed, Web of Science and Embase) was employed to identify observational studies on the associations of dietary vitamin A and beta-carotene intake with depression. The pooled relative risk (RR) of depression for the highest vs. lowest dietary vitamin A and beta-carotene intake category, and the standard mean difference (SMD) of dietary vitamin A and beta-carotene intake for depression vs. control subjects, were calculated.ResultsA total of 25 observational studies (100,955 participants), which included 24 cross-sectional/case-control and 1 prospective cohort study, were included in this study. The overall multi-variable adjusted RR demonstrated that dietary vitamin A intake was inversely associated with depression (RR = 0.83, 95%CI: 0.70–1.00; P = 0.05). In addition, the combined SMD showed that the dietary vitamin A intake in depression was also lower than that in control subjects (SMD = −0.13, 95%CI: −0.18 to −0.07; P < 0.001). On the other hand, the overall multi-variable adjusted RR indicated that dietary beta-carotene intake was negatively associated with depression (RR = 0.63, 95%CI: 0.55–0.72; P < 0.001). The combined SMD showed that the dietary beta-carotene intake in depression was also lower than that in control subjects (SMD = −0.34, 95%CI: −0.48 to −0.20; P < 0.001).ConclusionOur results suggest that both dietary vitamin A and beta-carotene intake is inversely associated with depression. However, due to the limited evidence, further prospective cohort studies are still needed.

show abstract

Nrf2 Alleviates Cognitive Dysfunction and Brain Inflammatory Injury via Mediating Wfs1 in Rats with Depression-Like Behaviors

Cited by 3 publications

References 40 publications

The Nrf2 Pathway in Depressive Disorders: A Systematic Review of Animal and Human Studies

The Nrf2 Pathway in Depressive Disorders: A Systematic Review of Animal and Human Studies

Research progress of miRNA in different depression model samples

Associations of Dietary Vitamin A and Beta-Carotene Intake With Depression. A Meta-Analysis of Observational Studies

Contact Info

Product

Resources

About