Sulforaphane mitigates LPS-induced neuroinflammation through modulation of Cezanne/NF-κB signalling

Wang, Zeng-chun; Chen, Qiang; Wang, Jing; Yu, Ling-Shan

doi:10.1016/j.lfs.2020.118519

Cited by 18 publications

(6 citation statements)

References 38 publications

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“…In addition, necroptosis predominated in mice stimulated with high doses of LPS compared with low doses of LPS (75), and stimulation with various PAMPs enhanced necroptosis in macrophages expressing the RIPK1 K45A mutation (79). Wang et al (80) found that upregulation of the deubiquitinating enzyme Cezanne in BV2 cells inhibited the NF-kB pathway, and inhibition of Cezanne was accompanied by increased levels of RIPK1 K63 ubiquitination. The importance of cell death in regulating systemic inflammation is highlighted by the RIPK1 knockout embryonic mice, which die during the embryonic stage due to systemic inflammation, and by blocking the necroptosis pathway and the MyD88 pathway reduce inflammation, but only mice with both RIPK3 and caspase-8 knockout survive after weaning (81).…”

Section: Roles and Mechanism Of Ripk1 In The Development Of Sepsismentioning

confidence: 99%

RIPK1 in the inflammatory response and sepsis: Recent advances, drug discovery and beyond

et al. 2023

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Cytokine storms are an important mechanism of sepsis. TNF-α is an important cytokine. As a regulator of TNF superfamily receptors, RIPK1 not only serves as the basis of the scaffold structure in complex I to promote the activation of the NF-κB and MAPK pathways but also represents an important protein in complex II to promote programmed cell death. Ubiquitination of RIPK1 is an important regulatory function that determines the activation of cellular inflammatory pathways or the activation of death pathways. In this paper, we introduce the regulation of RIPK1, RIPK1 PANoptosome’s role in Inflammatory and sepsis, and perspectives.

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Section: Roles and Mechanism Of Ripk1 In The Development Of Sepsismentioning

confidence: 99%

RIPK1 in the inflammatory response and sepsis: Recent advances, drug discovery and beyond

et al. 2023

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“…1 A). After exercise, the MWM test was performed to assess hippocampus-dependent spatial learning and memory ability (Wang et al 2020 ) to reveal the potential neuroprotective effects of exercise. The average escape latency of each group decreased during the training days.…”

Section: Resultsmentioning

confidence: 99%

Effects of exercise-targeted hippocampal PDE-4 methylation on synaptic plasticity and spatial learning/memory impairments in D-galactose-induced aging rats

Jin,

Li,

Wei

et al. 2023

Exp Brain Res

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Physical exercise reduces the effects of aging and cognitive decline by improving synaptic plasticity and spatial learning. However, the underlying neurobiological mechanisms are unclear. A total of 45 Male SPF Sprague–Dawley rats were acclimatized and then allocated into three groups, 15 in each group: the saline control (DC) group, D-gal-induced aging (DA) group, and D-gal-induced aging + exercise (DE) group. Six weeks of intraperitoneal injections of D-gal at a concentration of 100 mg/kg body weight/d was injected to establish model of aging in the DA and DE groups. Morris water maze test was implemented to evaluate the hippocampus related cognition. SOD activity and MDA was tested to assess the aging in all groups. H&E and Nissl staining was used to observe the histopathological changes of hippocampal neurons in aging rats. Quantitative real-time polymerase chain reaction, western blotting and immunofluorescence staining techniques were used to investigate the expression of synaptic genes and proteins in the hippocampus. Massarray methylation system was employed to measure the PDE-4 gene methylation level in rat hippocampal tissues. Our results demonstrated that exercise intervention improves cognitive function in D-gal-induced aging rats. The methylation of CpG sites in PDE-4 in the hippocampus was significantly increased. The physical exercise significantly increased PDE-4 gene methylation and effectively decreased PDE-4 gene and protein expression. These beneficial behavioral and morphological effects were attributed to PDE-4 methylation, which was activated cAMP/PKA/CREB pathway and improved synaptic plasticity. Exercise induced PDE-4 methylation is key mechanism underpinning the amelioration of learning/memory impairment, suggesting the potential efficacy of physical exercise training in delaying brain aging.

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“…Furthermore, LIPUS converts acoustic signals into mechanical signals, which then trigger a series of cellular responses [18,19]. For example, LIPUS has been reported to treat periodontitis and neurological diseases owing to its anti-inflammatory effect [20][21][22][23]. Notably, the effect of LIPUS in inhibiting apoptosis is remarkable, and LIPUS has shown positive effects on myocardial necrosis and nervous system diseases by inhibiting apoptosis of cardiomyocytes and neuronal cells [24,25].…”

Section: Introductionmentioning

confidence: 99%

Low-intensity pulsed ultrasound delays the progression of osteoarthritis by regulating the YAP–RIPK1–NF-κB axis and influencing autophagy

Pan,

Lu,

Hao

et al. 2024

J Transl Med

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Background Osteoarthritis (OA) is a degenerative disease characterized by chronic inflammation of the joint. As the disease progresses, patients will gradually develop symptoms such as pain, physical limitations and even disability. The risk factors for OA include genetics, gender, trauma, obesity, and age. Unfortunately, due to limited understanding of its pathological mechanism, there are currently no effective drugs or treatments to suspend the progression of osteoarthritis. In recent years, some studies found that low-intensity pulsed ultrasound (LIPUS) may have a positive effect on osteoarthritis. Nonetheless, the exact mechanism by which LIPUS affects osteoarthritis remains unknown. It is valuable to explore the specific mechanism of LIPUS in the treatment of OA. Methods In this study, we validated the potential therapeutic effect of LIPUS on osteoarthritis by regulating the YAP–RIPK1–NF-κB axis at both cellular and animal levels. To verify the effect of YAP on OA, the expression of YAP was knocked down or overexpressed by siRNA and plasmid in chondrocytes and adeno-associated virus was injected into the knee joint of rats. The effect of LIPUS was investigated in inflammation chondrocytes induced by IL-1β and in the post-traumatic OA model. Results In this study, we observed that YAP plays an important role in the development of osteoarthritis and knocking down of YAP significantly inhibited the inflammation and alleviated cartilage degeneration. We also demonstrated that the expression of YAP was increased in osteoarthritis chondrocytes and YAP could interact with RIPK1, thereby regulating the NF-κB signal pathway and influencing inflammation. Moreover, we also discovered that LIPUS decreased the expression of YAP by restoring the impaired autophagy capacity and inhibiting the binding between YAP and RIPK1, thereby delaying the progression of osteoarthritis. Animal experiment showed that LIPUS could inhibit cartilage degeneration and alleviate the progression of OA. Conclusions These results showed that LIPUS is effective in inhibiting inflammation and cartilage degeneration and alleviate the progression of OA. As a result, our results provide new insight of mechanism by which LIPUS delays the development of osteoarthritis, offering a novel therapeutic regimen for osteoarthritis.

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Sulforaphane mitigates LPS-induced neuroinflammation through modulation of Cezanne/NF-κB signalling

Cited by 18 publications

References 38 publications

RIPK1 in the inflammatory response and sepsis: Recent advances, drug discovery and beyond

RIPK1 in the inflammatory response and sepsis: Recent advances, drug discovery and beyond

Effects of exercise-targeted hippocampal PDE-4 methylation on synaptic plasticity and spatial learning/memory impairments in D-galactose-induced aging rats

Low-intensity pulsed ultrasound delays the progression of osteoarthritis by regulating the YAP–RIPK1–NF-κB axis and influencing autophagy

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