Lipopolysaccharide/D-galactosamine-induced acute liver injury could be attenuated by dopamine receptor agonist rotigotine via regulating NF-κB signaling pathway

Yue, Shumin; Wang, Tian; Yang, Yunqi; Fan, Yi; Zhou, Lin; Li, Mingan; Fu, Fenghua

doi:10.1016/j.intimp.2021.107798

Cited by 16 publications

(12 citation statements)

References 42 publications

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“…The previous study in our lab showed that rotigotine and RoMS had a protective effect on the LPS/D-galactosamine-induced acute liver failure, which is consistent with the main manifestations of clinical acute liver failure ( Nakama et al, 2001 ; Yue et al, 2021 ). There are differences between LPS-induced liver injury and LPS/D-galactosamine-induced liver injury.…”

Section: Discussionsupporting

confidence: 84%

“…Rotigotine extended-release microspheres (RoMS) is a sustained -release formulation that can release continuously rotigotine for more than 7 days in animals after a single dose of RoMS ( Lv et al, 2019 ; Li et al, 2022 ). We have previously demonstrated that RoMS alleviated inflammatory pain and alleviated LPS/D-galactosamine-induced acute liver injury in animals ( Li T. et al, 2021 ; Yue et al, 2021 ). DA and DRs agonists have shown better efficacy in inflammation-related diseases.…”

Section: Introductionmentioning

confidence: 99%

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Continuous Activation of Dopamine Receptors Alleviates LPS-Induced Liver Injury in Mice via β-arrestin2 Dependent Akt/NF-κB Pathway

Zhang

Zhou

et al. 2022

Front. Pharmacol.

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Many studies showed that dopamine receptors (DRs) agonists have anti-inflammatory effects. Rotigotine, a non-ergot dopamine receptor agonist, mainly actives DRD2/DRD3/DRD1. Rotigotine extended-release microspheres (RoMS) are a sustained-release formulation that can release sustainably rotigotine for more than 7 days after a single dose of RoMS. This study aimed to investigate whether RoMS can attenuate the lipopolysaccharide (LPS)-induced liver injury of mice. The liver injury was evaluated by assaying serum transaminase and observing histopathological changes. The levels of pro-inflammatory cytokines in serum were also detected. Western blot was employed to assay the expression of proteins in the Akt/NF-κB pathway. The results showed that pre-administration with a single dose of RoMS could inhibit the increase of serum transaminase induced by LPS, alleviate the pathological damage of liver tissue, and decrease the levels of tumor necrosis factor-α and interleukin-6. In addition, RoMS decreased Toll-like receptor 4 protein expression in liver tissue. RoMS mitigated liver injury by activating DRs and negatively regulating the β-arrestin2-dependent Akt/NF-κB signaling pathway. The effects of RoMS could be weakened or abolished by the specific DRD2 antagonist, R121. In conclusion, activation of DRs inhibited the releases of pro-inflammatory cytokines and alleviated the immune-mediated liver injury induced by LPS in mice. The anti-inflammatory mechanism of RoMS may be related to the regulation of the β-arrestin2-dependent Akt/NF-κB signaling pathway.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Continuous Activation of Dopamine Receptors Alleviates LPS-Induced Liver Injury in Mice via β-arrestin2 Dependent Akt/NF-κB Pathway

Zhang

Zhou

et al. 2022

Front. Pharmacol.

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“…β-arrestin2 acts as a G-protein-independent signaling mediator by scaffolding other proteins such as kinases and, in this way, regulate the Akt/NF-κB signaling pathway and inhibits the production of proinflammatory cytokines ( Beaulieu et al, 2007 ; Li et al, 2022 ). Another study reported that D2DR negatively regulates the Akt/NF-κB inflammatory signaling pathway and exerts protective effects against LPS liver injury by reducing the serum aminotransferases activity and TNF-α production ( Yue et al, 2021 ). Data presented here indicate that D2DR activation reduces the IL-1β, IL-6, and TNF-α production.…”

Section: Discussionmentioning

confidence: 99%

Activation of dopamine D2 receptors attenuates neuroinflammation and ameliorates the memory impairment induced by rapid eye movement sleep deprivation in a murine model

et al. 2022

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The proinflammatory state, which may be induced by sleep deprivation, seems to be a determining factor in the development of neurodegenerative processes. Investigations of mechanisms that help to mitigate the inflammatory effects of sleep disorders are important. A new proposal involves the neurotransmitter dopamine, which may modulate the progression of the immune response by activating receptors expressed on immune cells. This study aimed to determine whether dopamine D2 receptor (D2DR) activation attenuates the proinflammatory response derived from rapid eye movement (REM) sleep deprivation in mice. REM sleep deprivation (RSD) was induced in 2-month-old male CD1 mice using the multiple platform model for three consecutive days; during this period, the D2DR receptor agonist quinpirole (QUIN) was administered (2 mg/kg/day i.p.). Proinflammatory cytokine levels were assessed in serum and homogenates of the brain cortex, hippocampus, and striatum using ELISAs. Long-term memory deficits were identified using the Morris water maze (MWM) and novel object recognition (NOR) tests. Animals were trained until learning criteria were achieved; then, they were subjected to RSD and treated with QUIN for 3 days. Memory evocation was determined afterward. Moreover, we found RSD induced anhedonia, as measured by the sucrose consumption test, which is commonly related to the dopaminergic system. Our data revealed increased levels of proinflammatory cytokines (TNFα and IL-1β) in both the hippocampus and serum from RSD mice. However, QUIN attenuated the increased levels of these cytokines. Furthermore, RSD caused a long-term memory evocation deficit in both the MWM and NOR tests. In contrast, QUIN coadministration during the RSD period significantly improved the performance of the animals. On the other hand, QUIN prevented the anhedonic condition induced by RSD. Based on our results, D2DR receptor activation protects against memory impairment induced by disturbed REM sleep by inhibiting neuroinflammation.

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“…The transcription factor NF- κ B is central to the initiation and regulation of PRR-mediated inflammatory responses ( Liu et al, 2017 ), and the impact of dopamine on NF- κ B has been examined in a variety of immune cell subsets ( Takeuchi and Fukunaga, 2003 ; Zhang et al, 2015 ; Nolan et al, 2019 ; Wang, Chen et al, 2019 ; Wu et al, 2020 ; Yoshioka et al, 2020 ; Yue et al, 2021 ). A number of these studies suggest that dopamine inhibits NF- κ B, indicating anti-inflammatory activity.…”

Section: Dopamine and Immune Cellsmentioning

confidence: 99%

“…Although this study did not directly demonstrate that dopamine impacted NF- κ B, activation of this transcription factor is necessary for NLRP3 expression, and so the downregulation of NLRP3 indicates reductions in NF- κ B activity ( He et al, 2016 ; Herman and Pasinetti, 2018 ). Rotigotine (D2-like agonist) reduced TNF- α production and NF- κ B activation in a mouse model of acute liver injury ( Yue et al, 2021 ), and D2 signaling inhibited NF- κ B activation by inhibiting Akt in a murine model of acute pancreatitis ( Han et al, 2017 ). These effects are not unique to myeloid cells, as D2 activation in resting peripheral human T-cells was associated with IL-10 secretion, which regulates cytokine production via NF- κ B ( Besser et al, 2005 ).…”

Section: Dopamine and Immune Cellsmentioning

confidence: 99%

Dopamine, Immunity, and Disease

et al. 2022

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The neurotransmitter dopamine is a key factor in central nervous system (CNS) function, regulating many processes including reward, movement, and cognition. Dopamine also regulates critical functions in peripheral organs, such as blood pressure, renal activity, and intestinal motility. Beyond these functions, a growing body of evidence indicates that dopamine is an important immunoregulatory factor. Most types of immune cells express dopamine receptors and other dopaminergic proteins, and many immune cells take up, produce, store, and/or release dopamine, suggesting that dopaminergic immunomodulation is important for immune function. Targeting these pathways could be a promising avenue for the treatment of inflammation and disease, but despite increasing research in this area, data on the specific effects of dopamine on many immune cells and disease processes remain inconsistent and poorly understood. Therefore, this review integrates the current knowledge of the role of dopamine in immune cell function and inflammatory signaling across systems. We also discuss the current understanding of dopaminergic regulation of immune signaling in the CNS and peripheral tissues, highlighting the role of dopaminergic immunomodulation in diseases such as Parkinson’s disease, several neuropsychiatric conditions, neurologic human immunodeficiency virus, inflammatory bowel disease, rheumatoid arthritis, and others. Careful consideration is given to the influence of experimental design on results, and we note a number of areas in need of further research. Overall, this review integrates our knowledge of dopaminergic immunology at the cellular, tissue, and disease level and prompts the development of therapeutics and strategies targeted toward ameliorating disease through dopaminergic regulation of immunity. Significance Statement Canonically, dopamine is recognized as a neurotransmitter involved in the regulation of movement, cognition, and reward. However, dopamine also acts as an immune modulator in the central nervous system and periphery. This review comprehensively assesses the current knowledge of dopaminergic immunomodulation and the role of dopamine in disease pathogenesis at the cellular and tissue level. This will provide broad access to this information across fields, identify areas in need of further investigation, and drive the development of dopaminergic therapeutic strategies.

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Lipopolysaccharide/D-galactosamine-induced acute liver injury could be attenuated by dopamine receptor agonist rotigotine via regulating NF-κB signaling pathway

Cited by 16 publications

References 42 publications

Continuous Activation of Dopamine Receptors Alleviates LPS-Induced Liver Injury in Mice via β-arrestin2 Dependent Akt/NF-κB Pathway

Continuous Activation of Dopamine Receptors Alleviates LPS-Induced Liver Injury in Mice via β-arrestin2 Dependent Akt/NF-κB Pathway

Activation of dopamine D2 receptors attenuates neuroinflammation and ameliorates the memory impairment induced by rapid eye movement sleep deprivation in a murine model

Dopamine, Immunity, and Disease

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