Ginkgolide B attenuates myocardial infarction-induced depression-like behaviors via repressing IL-1β in central nervous system

Ge, Yali; Xu, Wan; Zhang, Lijun; Liu, Meiyan

doi:10.1016/j.intimp.2020.106652

Cited by 36 publications

(24 citation statements)

References 49 publications

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“…Moreover, emerging data have shown that plant-derived compounds can exert neuroprotective effects that prevent neurological disorders in depression. For instance, ganoderic acid A [ 227 ], asperosaponin VI [ 228 ], 20( S )-protopanaxadiol [ 229 ], scutellarin [ 230 ], astragalin [ 231 ], hesperidin [ 232 ], 5- O -methylvisammioside [ 233 ], ginkgolide B [ 234 ], leonurine [ 235 ], ferulic acid [ 236 ], and (+)-sesamin [ 69 ] were found to inactivate microglia in stress-induced depression models. Recent information concerning the antidepressant activity of phytochemicals through regulation of microglial polarization is illustrated in Table 2 .…”

Section: Introductionmentioning

confidence: 99%

Microglia in depression: an overview of microglia in the pathogenesis and treatment of depression

Wang

Sun

et al. 2022

J Neuroinflammation

230

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Major depressive disorder is a highly debilitating psychiatric disorder involving the dysfunction of different cell types in the brain. Microglia are the predominant resident immune cells in the brain and exhibit a critical role in depression. Recent studies have suggested that depression can be regarded as a microglial disease. Microglia regulate inflammation, synaptic plasticity, and the formation of neural networks, all of which affect depression. In this review, we highlighted the role of microglia in the pathology of depression. First, we described microglial activation in animal models and clinically depressed patients. Second, we emphasized the possible mechanisms by which microglia recognize depression-associated stress and regulate conditions. Third, we described how antidepressants (clinical medicines and natural products) affect microglial activation. Thus, this review aimed to objectively analyze the role of microglia in depression and focus on potential antidepressants. These data suggested that regulation of microglial actions might be a novel therapeutic strategy to counteract the adverse effects of devastating mental disorders.

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Section: Introductionmentioning

confidence: 99%

Microglia in depression: an overview of microglia in the pathogenesis and treatment of depression

Wang

Sun

et al. 2022

J Neuroinflammation

230

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“…IBM SPSS statistics software (version 24.0, IBM, Armonk, New York, USA) and GraphPad Prism Software (version 8.0.2, San Diego, CA, USA) were used for data analysis. Due to this was an exploratory study, we decided the sample size by considering scientific and qualitative levels and our former animal experiment experiences [ 10 , 13 , 14 ].…”

Section: Methodsmentioning

confidence: 99%

“…In addition, GBE could relieve atherosclerosis by decreasing plasma lipid via reducing the expression of connexin 43 protein [ 9 ]. In our previous research, we have demonstrated the promising effect of GBE and Ginkgo B in attenuating depressive behaviors in mice with myocardial infarction (MI) through inflammation suppression [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Ginkgo Biloba Extract Reduces Cardiac and Brain Inflammation in Rats Fed a HFD and Exposed to Chronic Mental Stress through NF-κB Inhibition

Zhang

Tao

et al. 2022

Mediators of Inflammation

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Background. Cardiac and brain inflammation can lead to a host of deleterious health effects. Our formal experimental research showed that Ginkgo Biloba Extract (GBE) contributed to the reduction of inflammation in mice with myocardial infarction along with depression. This study is aimed at expanding on these findings via analysis of the cardiac and brain inflammation, which was prevented by GBE in rats suffering with a high-fat diet (HFD) combined with unpredictable chronic mild stress (UCMS). Methods. Fifty male Wistar rats were randomly divided into 5 groups treated with normal diet, UCMS, HFD, HFD+UCMS, or HFD+UCMS+GBE respectively. Rats treated with HFD were fed a high-fat diet for 10 or 13 weeks. Rats treated with UCMS were exposed to 8 types of chronic physical and psychological stressors for 10 or 13 weeks. The HFD+UCMS+GBE group was given GBE via intragastric gavage for 8 consecutive weeks. Sucrose preference was established for the assessment of depressive behaviors. The heart function was evaluated by echocardiography. The rats were terminated at the end of the 10th or 13th week. The blood was used for detecting low-density lipoprotein cholesterol (LDL-c) and total cholesterol (TCHO) by the kit instructions; Helper T Lymphocytes (TH cells, CD3+CD4+) by flow cytometry; and Interleukin- (IL-) 1β, IL-37, IL-38, NT-proBNP, hs-cTNI, and Ischemia-modified albumin (IMA) by enzyme-linked immunosorbent assay (ELISA). The cardiac tissues were used for detecting IL-1β, nuclear factor kappa B (NF-κB), inhibitor molecule protein (IκB), and IL-1 receptor (IL-1R) by ELISA and P65, P-P65, IκB, and phosphorylated inhibitor molecule protein α (P-IκBα) for western blotting. Cortex tissues were used for detecting 8-iso-prostaglandinF2α (8-iso-PGF2α) by ELISA. Oil Red staining was carried out to evaluate the lipid deposits in the rats’ aortic arteries. Sirius Red staining was performed to display collagen fibers in the arteries. Hematoxylin and Eosin (HE) staining was applied to reveal pathological changes to arteries and cardiac tissue. Immunohistochemical staining was employed to assess the distribution of inflammatory cytokine IL-1β in arteries and cardiac tissues. Transmission Electron Microscopy (TEM) was performed to observe the ultrastructure of hippocampal cornu ammonis (CA)1 (CA1) neurons. Results. In the rats with HFD+UCMS+GBE, over 13 weeks, GBE exerted a protective role of both the heart and brain, by attenuating cardiac inflammation and brain oxidative stress. Levels of Helper T lymphocytes and serum anti-inflammatory cytokines involving IL-37 and IL-38 were all elevated, and the depressive behaviors of HFD+UCMS rats were attenuated by GBE. This protective role was accomplished via inhibition of the canonical NF-κB signaling pathway, through downregulation of the expressions of P-P65 and P-IκB-α in the heart, hippocampus, cortex, and hypothalamus. Conclusions. This study suggests that GBE poses a protective role from the various pathologies associated with high-fat diets, unpredictable chronic mild stress, and depression, possibly via improving peripheral immunity and reducing cardiac and brain inflammation.

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“…Currently, Ginkgo biloba is an adaptive species and grows well in most parts of the world, including in the Mediterranean climate. The extract of Ginkgo biloba and/or its ginkgolide components, e.g., EGb761, BN52021, BN5739 and BN52063, possess many beneficial effects on the function of several injured and diseased cells and organs, including the nervous [116][117][118][119][120], renal [121][122][123] and cardiovascular [124][125][126][127][128][129][130] systems.…”

Section: Ginkgo Biloba "Ginkgoflavonoids" and Ho-1mentioning

confidence: 99%

Heme Degradation in Pathophysiology of and Countermeasures to Inflammation-Associated Disease

Haines

Tósaki

2020

IJMS

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The class of tetrapyrrol “coordination complexes” called hemes are prosthetic group components of metalloproteins including hemoglobin, which provide functionality to these physiologically essential macromolecules by reversibly binding diatomic gasses, notably O2, which complexes to ferrous (reduced/Fe(II)) iron within the heme porphyrin ring of hemoglobin in a pH- and PCO2-dependent manner—thus allowing their transport and delivery to anatomic sites of their function. Here, pathologies associated with aberrant heme degradation are explored in the context of their underlying mechanisms and emerging medical countermeasures developed using heme oxygenase (HO), its major degradative enzyme and bioactive metabolites produced by HO activity. Tissue deposits of heme accumulate as a result of the removal of senescent or damaged erythrocytes from circulation by splenic macrophages, which destroy the cells and internal proteins, including hemoglobin, leaving free heme to accumulate, posing a significant toxicogenic challenge. In humans, HO uses NADPH as a reducing agent, along with molecular oxygen, to degrade heme into carbon monoxide (CO), free ferrous iron (FeII), which is sequestered by ferritin protein, and biliverdin, subsequently metabolized to bilirubin, a potent inhibitor of oxidative stress-mediated tissue damage. CO acts as a cellular messenger and augments vasodilation. Nevertheless, disease- or trauma-associated oxidative stressors sufficiently intense to overwhelm HO may trigger or exacerbate a wide range of diseases, including cardiovascular and neurologic syndromes. Here, strategies are described for counteracting the effects of aberrant heme degradation, with a particular focus on “bioflavonoids” as HO inducers, shown to cause amelioration of severe inflammatory diseases.

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Ginkgolide B attenuates myocardial infarction-induced depression-like behaviors via repressing IL-1β in central nervous system

Cited by 36 publications

References 49 publications

Microglia in depression: an overview of microglia in the pathogenesis and treatment of depression

Microglia in depression: an overview of microglia in the pathogenesis and treatment of depression

Ginkgo Biloba Extract Reduces Cardiac and Brain Inflammation in Rats Fed a HFD and Exposed to Chronic Mental Stress through NF-κB Inhibition

Heme Degradation in Pathophysiology of and Countermeasures to Inflammation-Associated Disease

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