Ginsenoside Rh2 reduces depression in offspring of mice with maternal toxoplasma infection during pregnancy by inhibiting microglial activation via the HMGB1/TLR4/NF-κB signaling pathway

Xu, Xiang; Lu, Yu-Nan; Cheng, Jia-Hui; Lan, Hui-Wen; Lu, Jing-Mei; Jin, Guang-Nan; Xu, G.; Jin, Changchun; Ma, Juan; Piao, Hu-Nan; Jin, Xuejun; Li, Piao

doi:10.1016/j.jgr.2021.04.003

Cited by 22 publications

(15 citation statements)

References 43 publications

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“…SAG1 is often used as a toxoplasma tachyzoite specific marker to analyse parasite loads in various organs by using QC-PCR targeting SAG1 gene. 10,44,45,65 In this study, we detected a large numbers of T. gondii in the BV2 cells and MLN or brain tissues by the QC-PCR method. However, the T. gondii abundance was significantly reduced after SERT or SD (SD-Na) treatment.…”

Section: Discussionmentioning

confidence: 72%

New role of sertraline against Toxoplasma gondii‐induced depression‐like behaviours in mice

Lan

Zhao

et al. 2021

Parasite Immunology

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Toxoplasma gondii (T. gondii) infection is a risk factor for the development of some neuropsychiatric diseases. 1 Numerous clinical studies have shown that the seroprevalence of T. gondii is associated with a variety of neuropsychiatric conditions, including schizophrenia, 2 suicidal behaviour, 2 mixed anxiety and depressive disorder. [3][4][5][6][7] T. gondii infection affects the predisposition and severity of depression in children and adolescents. 8 In our recent study, mice were also found to exhibit depression-like behaviours in a mouse model of T. gondii infection 9 or in offspring of mice with maternal T. gondii infection during pregnancy. 10 However, another study did not find a relationship between toxoplasmosis and major depression disorder. 11 Numerous studies have explored the causes of this controversy, that is, whether T. gondii infection induces mental disorder and whether this is affected by the host genetic susceptibility, 12 age of first exposure to T. gondii, 13 T. gondii strain 14 and symptom severity. 15 Interestingly, a case report of a T. gondii-seropositive depressed patient has shown that antidepressant treatment can be improved only after appropriate treatment for toxoplasmosis. 16 Thus, further research is required to examine the correlation between T. gondii infection and depression-like behaviours, to elucidate the exact mechanisms of depression-like behaviours caused by T. gondii infection, and to identify suitable drugs for treatment.

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Section: Discussionmentioning

confidence: 72%

New role of sertraline against Toxoplasma gondii‐induced depression‐like behaviours in mice

Lan

Zhao

et al. 2021

Parasite Immunology

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“…In the meantime, it is widely accepted that HMGB1 release mediates hippocampal inflammation and contributes to cognitive impairment in preclinical models [ 56 , 57 , 58 , 59 ]. Intervention targeting the HMGB1/TLR4/NF-κB pathway could alleviate neuroinflammation and improve cognitive impairment in models of depression, cognitive impairment caused by high-fat and high-sugar diets, and traumatic brain injury [ 57 , 60 , 61 , 62 ]. Blocking HMGB1/RAGE signaling by Berberine also alleviates SAE’s cognitive deficits [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Alleviates Neuroinflammation by Inhibiting the HMGB1 Signaling Pathway in Rats with Sepsis-Associated Encephalopathy

et al. 2022

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Sepsis-Associated Encephalopathy (SAE) is common in sepsis patients, with high mortality rates. It is believed that neuroinflammation is an important mechanism involved in SAE. High mobility group box 1 protein (HMGB1), as a late pro-inflammatory factor, is significantly increased during sepsis in different brain regions, including the hippocampus. HMGB1 causes neuroinflammation and cognitive impairment through direct binding to advanced glycation end products (RAGE) and Toll-like receptor 4 (TLR4). Electroacupuncture (EA) at Baihui (GV20) and Zusanli (ST36) is beneficial for neurological diseases and experimental sepsis. Our study used EA to treat SAE induced by lipopolysaccharide (LPS) in male Sprague–Dawley rats. The Y maze test was performed to assess working memory. Immunofluorescence (IF) and Western blotting (WB) were used to determine neuroinflammation and the HMGB1 signaling pathway. Results showed that EA could improve working memory impairment in rats with SAE. EA alleviated neuroinflammation by downregulating the hippocampus’s HMGB1/TLR4 and HMGB1/RAGE signaling, reducing the levels of pro-inflammatory factors, and relieving microglial and astrocyte activation. However, EA did not affect the tight junctions’ expression of the blood–brain barrier (BBB) in the hippocampus.

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“…Brain-resident cells (most likely microglia) can produce IFN-γ and thereby can inhibit T. gondii replication in the brain, while activating astrocyte cells to produce chemokines CXC ligand (CXCL) 9 and CXCL10 to recruit immune cells (such as CD4 + T cells) from the peripheral blood to the CNS ( Schluter and Barragan, 2019 ; Suzuki, 2020 ). Pharmacological studies have found that arctigenin (AG) and ginsenoside Rh2 (GRh2) can ameliorate host or host offspring MDD caused by T. gondii infection, mainly because AG and GRh2 can inhibit microglia activation and neuroinflammation via the TLR4/NF-κB, TNF receptor 1 (TNFR1)/NF-κB signaling pathways and high mobility group box 1 (HMGB1)/TLR4/NF-κB signaling pathway, respectively ( Cheng et al., 2020 ; Xu et al., 2022 ).…”

Section: T Gondii Marches To the Brainmentioning

confidence: 99%

From the immune system to mood disorders especially induced by Toxoplasma gondii: CD4+ T cell as a bridge

Wang

Zhong

Chen

et al. 2023

Front. Cell. Infect. Microbiol.

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Toxoplasma gondii (T. gondii), a ubiquitous and obligatory intracellular protozoa, not only alters peripheral immune status, but crosses the blood-brain barrier to trigger brain parenchymal injury and central neuroinflammation to establish latent cerebral infection in humans and other vertebrates. Recent findings underscore the strong correlation between alterations in the peripheral and central immune environment and mood disorders. Th17 and Th1 cells are important pro-inflammatory cells that can drive the pathology of mood disorders by promoting neuroinflammation. As opposed to Th17 and Th1, regulatory T cells have inhibitory inflammatory and neuroprotective functions that can ameliorate mood disorders. T. gondii induces neuroinflammation, which can be mediated by CD4+ T cells (such as Tregs, Th17, Th1, and Th2). Though the pathophysiology and treatment of mood disorder have been currently studied, emerging evidence points to unique role of CD4+ T cells in mood disorder, especially those caused by T. gondii infection. In this review, we explore some recent studies that extend our understanding of the relationship between mood disorders and T. gondii.

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Ginsenoside Rh2 reduces depression in offspring of mice with maternal toxoplasma infection during pregnancy by inhibiting microglial activation via the HMGB1/TLR4/NF-κB signaling pathway

Cited by 22 publications

References 43 publications

New role of sertraline against Toxoplasma gondii‐induced depression‐like behaviours in mice

New role of sertraline against Toxoplasma gondii‐induced depression‐like behaviours in mice

Electroacupuncture Alleviates Neuroinflammation by Inhibiting the HMGB1 Signaling Pathway in Rats with Sepsis-Associated Encephalopathy

From the immune system to mood disorders especially induced by Toxoplasma gondii: CD4+ T cell as a bridge

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