Trans-cinnamaldehyde improves neuroinflammation-mediated NMDA receptor dysfunction and memory deficits through blocking NF-κB pathway in presenilin1/2 conditional double knockout mice

Zhao, Yang; Deng, Hongping; Li, Kun; Wang, Lijun; Wu, Yongkang; Dong, Xianwen; Wang, Xingyu; Chen, Yongjun; Xu, Ying

doi:10.1016/j.bbi.2019.07.032

Cited by 31 publications

(37 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Increasing evidence indicates that neuroin ammation may play a crucial role in the development of memory de cits [36,37]. It has been reported that the ROS system is associated with the pathology that results from neuroin ammation [38].…”

Section: Discussionmentioning

confidence: 99%

Pharmacological activation of GPR55 improved cognitive impairment, neuroinflammation, oxidative stress and apoptosis induced by lipopolysaccharide in mice

Wang

Xiang

et al. 2020

Preprint

View full text Add to dashboard Cite

BackgroundNeuroinflammation, oxidative stress and apoptosis are implicated in the pathogenesis of Alzheimer’s disease (AD). The purpose of the present study was to investigate the neuroprotective effects and possible mechanism of G-protein coupled receptor 55 (GPR55) agonist, O-1602, on lipopolysaccharide (LPS)-induced cognitive deficits in mice. MethodsICR mice were treated with intracerebroventricular (i.c.v.) injection of LPS. Cognitive tests were performed, including the open field, Morris water maze, novel object recognition, and passive avoidance tests. The expression of GPR55, NF-κB p65, caspase-3, Bax and Bcl-2 were examined in the hippocampus by western blotting. Pro-inflammatory cytokines and microglia were detected by ELISA kit and immunohistochemical analyses, respectively. The malondialdehyde (MDA) level, and superoxide dismutase (SOD) activity were examined by assay kits. Furthermore, TUNEL-staining was used to detect neuronal apoptosis.ResultsI.c.v. injection of LPS exhibited impaired performance in the behavior tests, which were ameliorated by O-1602 treatment(2.0 or 4.0 μg/mouse, i.c.v.). Importantly, O-1602 reversed GPR55 down-regulation, decreased the expression of NF-κB p65, and suppressed the accumulation of pro-inflammatory cytokines and microglia activation, decreased malondialdehyde (MDA) level, and increased superoxide dismutase (SOD) activity. In addition, O-1602 also significantly decreased Bax and increased Bcl-2 expression as well as decreased caspase-3 activity and TUNEL-positive cells, suppressed neuronal apoptosis in the hippocampus of LPS-treated mice.Conclusionswe conclude that O-1602 may ameliorate LPS-induced cognition deficits via inhibiting neuroinflammation, oxidative stress and apoptosis mediated by NF-κB signaling in mice.

show abstract

Section: Discussionmentioning

confidence: 99%

Pharmacological activation of GPR55 improved cognitive impairment, neuroinflammation, oxidative stress and apoptosis induced by lipopolysaccharide in mice

Wang

Xiang

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…The experiment was performed as we previously described [ 27 ], and each mouse was placed in a new object recognition box (40 cm × 40 cm × 25 cm) for 3 days to adapt to the environment. During the training phase, two toys with the same color and shape were placed in the experimental box, and each group of mice was allowed to explore freely for 15 min.…”

Section: Methodsmentioning

confidence: 99%

Electroacupuncture Ameliorates Neuroinflammation-Mediated Cognitive Deficits through Inhibition of NLRP3 in Presenilin1/2 Conditional Double Knockout Mice

Shi

Zhao

et al. 2021

Neural Plasticity

Self Cite

View full text Add to dashboard Cite

Neuroinflammation is considered as one of the crucial pathogenesis in promoting neurodegenerative progress of Alzheimer’s disease (AD). As complementary and alternative therapy, electroacupuncture (EA) stimulation has been widely used in clinical practice for anti-inflammation. However, whether EA promotes the cognitive deficits resulting from neuroinflammation in AD remains unclear. In this study, the presenilin 1 and 2 conditional double knockout (PS cDKO) mice, exhibited a series of AD-like pathology, robust neuroinflammatory responses, and memory deficits, were used to evaluate the potential neuroprotective effect of EA at Baihui (GV 20) and Shenting (GV 24) by behavioral testing, electrophysiology recording, and molecular biology analyzing. First, we observed that EA improved memory deficits and impaired synaptic plasticity. Moreover, EA possesses an ability to suppress the hyperphosphorylated tau and robust elevated NLRP3, ASC, Caspase-1, IL-1β, and IL-18 in PS cDKO mice. Importantly, MCC950, a potent and selective inhibitor of NLPR3 inflammasome, has similar effects on inhibiting the hyperphosphorylated tau and the robust elevated NLRP3 components and neuroinflammatory responses of PS cDKO mice as well as EA treatment. Furthermore, EA treatment is not able to further improve the AD-like phenotypes of PS cDKO mice in combination with the MCC950 administration. Therefore, EA stimulation at GV 20 and GV 24 acupoints may be a potential alternative therapy for deterring cognitive deficits in AD through suppression of NLRP3 inflammasome activation.

show abstract

“…Trans-cinnamaldehyde, a primary bioactive component derived from the stem bark of Cinnamomum cassia, suppresses neuroinflammatory responses by diminishing microglial activation and levels of pro-inflammatory mediators. This reduces memory deficits in mice with Alzheimer's disease (Zhao et al, 2019). Gut microbial dysbiosis is involved in Parkinson's disease pathogenesis, and fecal microbiota transplantation can protect affected mice by suppressing neuroinflammation and reducing TLR4/TNF-α signaling in microglia (Sun et al, 2018).…”

Section: Microglia and Stress Depression And Psychological Disordersmentioning

confidence: 99%

Psychoneuroimmunology goes East: Development of the PNIRS affiliate and its expansion into PNIRS

Kelley

Peng

Liu

et al. 2020

Brain, Behavior, and Immunity

View full text Add to dashboard Cite

Trans-cinnamaldehyde improves neuroinflammation-mediated NMDA receptor dysfunction and memory deficits through blocking NF-κB pathway in presenilin1/2 conditional double knockout mice

Cited by 31 publications

References 54 publications

Pharmacological activation of GPR55 improved cognitive impairment, neuroinflammation, oxidative stress and apoptosis induced by lipopolysaccharide in mice

Pharmacological activation of GPR55 improved cognitive impairment, neuroinflammation, oxidative stress and apoptosis induced by lipopolysaccharide in mice

Electroacupuncture Ameliorates Neuroinflammation-Mediated Cognitive Deficits through Inhibition of NLRP3 in Presenilin1/2 Conditional Double Knockout Mice

Psychoneuroimmunology goes East: Development of the PNIRS affiliate and its expansion into PNIRS

Contact Info

Product

Resources

About