Activation of monoaminergic system contributes to the antidepressant- and anxiolytic-like effects of J147

Pan, Xiaoyu; Chen, Ling; Xu, Weijie; Bao, Shaowen; Wang, Jun; Cui, Xiao; Gao, Shichao; Liu, Kaiping; Avasthi, Shivani; Zhang, Meixi; Chen, Ruijie

doi:10.1016/j.bbr.2021.113374

Cited by 15 publications

(13 citation statements)

References 36 publications

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“…Only one study found no improvements in anxiety, as measured by the open field and elevated plus maze tests, nor in “depressive-like” states, as measured by the forced swimming test [ 89 ]. Another study found no improvements in anhedonia, as measured by the sucrose preference test [ 86 ].…”

Section: Resultsmentioning

confidence: 99%

“…Besides, fifteen studies reported an increased level of DA [ 38 , 41 , 42 , 44 , 45 , 46 , 48 , 49 , 55 , 72 , 77 , 81 , 87 , 91 ]. NA was also incremented in five studies [ 46 , 49 , 55 , 63 , 86 ]. In addition, curcumin has been claimed to present beneficial effects on reducing inflammatory cytokines (IL-1β, IL-6) [ 60 , 63 , 69 , 70 , 71 , 76 , 77 , 91 ], reducing the NF-κB-iNOS-COX-2-TNF-α inflammatory signaling pathway [ 39 , 51 , 52 ], and modulating the levels of antioxidant markers, such as monoamine oxidase (MAO), malondialdehyde (MDA), CAT, or SOD [ 43 , 56 , 57 , 62 , 65 , 66 , 82 , 84 , 88 ].…”

Section: Resultsmentioning

confidence: 99%

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An Update on the Exploratory Use of Curcumin in Neuropsychiatric Disorders

et al. 2022

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Curcumin is a polyphenol extracted from the rhizome of the turmeric plant. Beyond its common use as a culinary spice in Eastern Asia, curcumin has been proposed as a therapeutic compound due to its antioxidant, anti-inflammatory and neuroprotective properties. Thus, its efficacy has been evaluated in various inflammatory-based psychiatric disorders, such as schizophrenia, depression, or autism. Our aim is to review those preclinical and clinical studies carried out in psychiatric disorders whose therapeutic approach has involved the use of curcumin and, therefore, to discern the possible positive effect of curcumin in these disorders. Preclinical studies and completed clinical trials of curcumin for psychiatric disorders published from January 2005 to October 2021 were identified through searching relevant databases until 31st October 2021. Sixty-five preclinical studies and 15 clinical trials and open-label studies were selected. Results showed a bias toward studies in depression and, to a lesser extent, schizophrenia. In all disorders, the results were positive in reducing psychiatric deficits. Despite the considerable number of beneficial outcomes reported, the small number of trials and the heterogeneity of protocols make it difficult to draw solid conclusions about the real potency of curcumin in psychiatric disorders.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

An Update on the Exploratory Use of Curcumin in Neuropsychiatric Disorders

et al. 2022

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“…After administration, rats were again placed in the glass cylinder for swimming for 5 min, and the immobility time within 5 min was observed and recorded ( Rao et al, 2021 ). Immobility time was defined as the time when the rat stopped struggling, floated in the water, and remained motionless, or only made necessary light movements to keep its head afloat in the water ( Porsolt et al, 1977 ; Pan et al, 2021 ).…”

Section: Methodsmentioning

confidence: 99%

Effects of Chang-Kang-Fang Formula on the Microbiota-Gut-Brain Axis in Rats With Irritable Bowel Syndrome

et al. 2022

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Chang-Kang-Fang formula (CKF), a multi-herb traditional Chinese medicine, has been used in clinical settings to treat irritable bowel syndrome (IBS). Recent studies show that 5.0 g/kg/d CKF can alleviate the symptoms of IBS rats by modulating the brain-gut axis through the production of brain-gut peptides (BGPs), thus relieving pain, and reversing the effects of intestinal propulsion disorders. However, the exact mechanisms underlying the therapeutic effects of CKF in IBS remain unclear. The microbiota-gut-brain axis (MGBA) is central to the pathogenesis of IBS, regulating BGPs, depression-like behaviors, and gut microbiota. Given that CKF ameliorates IBS via the MGBA, we performed metabolomic analyses, evaluated the gut microbiota, and system pharmacology to elucidate the mechanisms of action of CKF. The results of intestinal tract motility, abdominal withdrawal reflex (AWR), sucrose preference test (SPT), and the forced swimming test (FST) showed that the male Sprague–Dawley rats subjected to chronic acute combining stress (CACS) for 22 days exhibited altered intestinal motility, visceral hypersensitivity, and depression-like behaviors. Treatment of IBS rats with CKF normalized dysfunctions of CACS-induced central and peripheral nervous system. CKF regulated BDNF and 5-HT levels in the colon and hippocampus as well as the expressions of the related BGP pathway genes. Moreover, the system pharmacology assays were used to assess the physiological targets involved in the action of CKF, with results suggesting that CKF putatively functioned through the 5-HT-PKA-CREB-BDNF pathway. LC-MS-based metabolomics identified the significantly altered 5-HT pathway-related metabolites in the CKF treatment group, and thus, the CKF-related signaling pathways were further examined. After pyrosequencing-based analysis of bacterial 16S rRNA (V3 + V4 region) using rat feces, the Lefse analysis of gut microbiota suggested that CKF treatment could induce structural changes in the gut microbiota, thereby regulating it by decreasing Clostridiales, and the F-B ratio while increasing the levels of Lactobacillus. Furthermore, the integrated analysis showed a correlation of CKF-associated microbes with metabolites. These findings showed that CKF effectively alleviated IBS, which was associated with the altered features of the metabolite profiles and the gut microbiota through a bidirectional communication along the microbiota-gut-brain axis.

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“…To date, much progress has been made in the study of the potential etiology of depression, such as the involvement of monoamine neurotransmitters (serotonin, norepinephrine and dopamine) [ 4 ], brain-derived neurotrophic factor (BDNF) [ 5 ], hypothalamic-pituitary-adrenal (HPA) axis [ 6 ], corticotrophin releasing hormone (CRH) [ 7 ], chronic systemic inflammation [ 8 ], glutamate metabolism [ 9 ], neuronal synaptic plasticity [ 10 ] and oxidative stress [ 11 ] et al Research showed that serotonin deficiency may lead to the incidence of depression [ 12 ], which is currently one of the generally accepted hypotheses. The decrease of norepinephrine and dopamine in the blood and cerebrospinal fluid of patients with depression suggests a relationship between depression and monoamine neurotransmitters [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Potential biomarkers: differentially expressed proteins of the extrinsic coagulation pathway in plasma samples from patients with depression

Zhang

Shi

et al. 2021

Bioengineered

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Depression is a severe disabling psychiatric illness and the pathophysiological mechanisms remain unknown. In previous work, we found the changes in extrinsic coagulation (EC) pathway proteins in depressed patients compared with healthy subjects were significant. In this study, we screened differentially expressed proteins (DEPs) in the EC pathway, and explored the molecular mechanism by constructing a protein-protein interaction (PPI) network. The DEPs of the EC pathwaywere initially screened by isobaric tags for relative and absolute quantification (iTRAQ) in plasma samples obtained from 20 depression patients and 20 healthy controls, and were then identified by Enzyme-linked immunosorbent assays (ELISAs). Ingenuity Pathway Analysis (IPA) software was used to analyse pathway. The differentially expressed genes (DEGs) were identified by analyzing the GSE98793 microarray data from the Gene Expression Omnibus database using the Significance Analysis for Microarrays (SAM, version 4.1) statistical method. Cytoscape version 3.4.0 software was used to construct and visualize PPI networks. The results show that Fibrinogen alpha chain (FGA), Fibrinogen beta chain (FGB), Fibrinogen gamma chain (FGG) and Coagulation factor VII (FVII) were screened in the EC pathway from depression patient samples. FGA, FGB, and FGG were significantly up-regulated, and FVII was down-regulated. Thirteen DEGs related to depression and EC pathways were identified from the microarray database. Among them NF-κB Inhibitor Beta (NFKBIB) and Heat shock protein family B (small) member 1 (HSPB1) were highly correlated with EC pathway. We conclude that EC pathway is associated with depression, which provided clues for the biomarker development and the pathogenesis of depression.

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Activation of monoaminergic system contributes to the antidepressant- and anxiolytic-like effects of J147

Cited by 15 publications

References 36 publications

An Update on the Exploratory Use of Curcumin in Neuropsychiatric Disorders

An Update on the Exploratory Use of Curcumin in Neuropsychiatric Disorders

Effects of Chang-Kang-Fang Formula on the Microbiota-Gut-Brain Axis in Rats With Irritable Bowel Syndrome

Potential biomarkers: differentially expressed proteins of the extrinsic coagulation pathway in plasma samples from patients with depression

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