Silibinin rescues learning and memory deficits by attenuating microglia activation and preventing neuroinflammatory reactions in SAMP8 mice

Jin, Ge; Bai, Dafeng; Yin, Shankai; Yang, Zhipeng; Zou, Dan; Zhang, Zhong; Li, Xiaoxiu; Sun, Yuena; Zhu, Qing

doi:10.1016/j.neulet.2016.06.008

Cited by 53 publications

(20 citation statements)

References 27 publications

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“…The results of a meta-analysis showed that depression is accompanied by activation of the inflammatory response (Dowlati et al, 2010), and a review reported that the inflammatory response is one of the key factors in development of depression (Maes, 2011). Another study revealed a close relation between memory deficit and inflammation (Imamura et al, 2011; Jin et al, 2016). A few experimental studies have indicated that NLRP3 inflammasome activation in mononuclear blood cells is associated with depression, and could be a new target for depressive disorders (Alcocer-Gómez et al, 2014; Alcocer-Gomez and Cordero, 2014; Zhang et al, 2014).…”

Section: Discussionmentioning

confidence: 95%

“…LPS enhances peripheral NLRP3 inflammasome expression, which, in turn, aggravates the peripheral inflammatory response (Inoue et al, 2015; Zhang et al, 2015). LPS alone or peripheral inflammatory factors induced by LPS can trigger NLRP3 inflammasome activation in the central nervous system and may cause long-term behavioral alterations (Maes, 2011; Jin et al, 2016; Liu et al, 2016; Shi et al, 2016; Wang et al, 2016). Inflammasome activation is an important step in the development of systemic and brain inflammation.…”

Section: Discussionmentioning

confidence: 99%

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NLRP3 inflammasome activation contributes to long-term behavioral alterations in mice injected with lipopolysaccharide

et al. 2017

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Lipopolysaccharide (LPS) might affect the central nervous system by causing neuroinflammation, which subsequently leads to brain damage and dysfunction. In this study, we evaluated the role of nod-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome activation in long-term behavioral alterations of 8-week-old male C57BL/6 mice injected intraperitoneally with LPS (5 mg/kg). At different time points after injection, we assessed locomotor function with a 24-point neurologic deficit scoring system and the rotarod test; assessed recognition memory with the novel object recognition test; and assessed emotional abnormality (anhedonia and behavioral despair) with the tail suspension test, forced swim test, and sucrose preference test. We also assessed protein expression of NLRP3, apoptosis-associated speck-like protein (ASC), and caspase-1 p10 in hippocampus by Western blotting; measured levels of interleukin (IL)-1β, IL-18, tumor necrosis factor α (TNFα), and IL-10 in hippocampus; measured TNFα and IL-1β in serum by ELISA; and evaluated microglial activity in hippocampus by Iba1 immunofluorescence. We found that LPS-injected mice displayed long-term depression-like behaviors and recognition memory deficit; elevated expression of NLRP3, ASC, and caspase-1 p10; increased levels of IL-1β, IL-18, and TNFα; decreased levels of IL-10; and increased microglial activation. These effects were blocked by the NLRP3 inflammasome inhibitor Ac-Tyr-Val-Ala-Asp-chloromethylketone. The results demonstrate proof of concept that NLRP3 inflammasome activation contributes to long-term behavioral alterations in LPS-exposed mice, probably through enhanced inflammation, and that NLRP3 inflammasome inhibition might alleviate peripheral and brain inflammation and thereby ameliorate long-term behavioral alterations in LPS-exposed mice.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

NLRP3 inflammasome activation contributes to long-term behavioral alterations in mice injected with lipopolysaccharide

et al. 2017

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“…The temporal order memory, novel object recognition, and Y-maze tests were performed to examine dietary effects on spatial and recognition memory based on methods previously described (Jin et al, 2016;Uribe-Marino et al, 2016;Zhang et al, 2019). In the temporal order memory test, the discrimination index was calculated as [(Time with the older object -Time with recent object)/Total time with both objects] × 100.…”

Section: Behavioral Testingmentioning

confidence: 99%

Curdlan Prevents the Cognitive Deficits Induced by a High-Fat Diet in Mice via the Gut-Brain Axis

et al. 2020

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A high-fat (HF) diet is a major predisposing factor of neuroinflammation and cognitive deficits. Recently, changes in the gut microbiota have been associated with neuroinflammation and cognitive impairment, through the gut-brain axis. Curdlan, a bacterial polysaccharide widely used as food additive, has the potential to alter the composition of the microbiota and improve the gut-brain axis. However, the effects of curdlan against HF diet-induced neuroinflammation and cognitive decline have not been investigated. We aimed to evaluate the neuroprotective effect and mechanism of dietary curdlan supplementation against the obesity-associated cognitive decline observed in mice fed a HF diet. C57Bl/6J male mice were fed with either a control, HF, or HF with curdlan supplementation diets for 7 days (acute) or 15 weeks (chronic). We found that acute curdlan supplementation prevented the gut microbial composition shift induced by HF diet. Chronic curdlan supplementation prevented cognitive declines induced by HF diet. In addition, curdlan protected against the HF diet-induced abnormities in colonic permeability, hyperendotoxemia, and colonic inflammation. Furthermore, in the prefrontal cortex (PFC) and hippocampus, curdlan mitigated microgliosis, neuroinflammation, and synaptic impairments induced by a HF diet. Thus, curdlan-as a food additive and prebiotic-can prevent cognitive deficits induced by HF diet via the colon-brain axis.

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“…The Y-maze test was performed based on methods previously described [22]. After acclimatization of the mice, label the arms of the maze with different pictures.…”

Section: Behavioral Testingmentioning

confidence: 99%

β-glucan from Lentinula Edodes Prevents Cognitive Impairments in High-Fat Diet-Induced Obese Mice: Involvement of Colon-Brain Xxis

Pan

Jiang

Zhao

et al. 2020

Preprint

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Background: Long-term high fat (HF) diet intake can cause neuroinflammation and cognitive decline through the gut-brain axis. (1, 3)/(1, 6)-β-glucan, an edible polysaccharide isolated from medical mushroom, Lentinula edodes (L. edodes), has the potential to remodel gut microbiota. However, the effects of L. edode derived β-glucan against HF diet-induced neuroinflammation and cognitive decline remain unknown. This study aimed to evaluate the neuroprotective effect and mechanism of dietary L edodes β-glucan supplementation against the obesity-associated cognitive decline in mice fed by a HF diet. Methods: C57BL/6J male mice were fed with either a lab chow (LC), HF or HF with L. edodes β-glucan supplementation diets for 7 days (acute) or 15 weeks (chronic). Cognitive behavior was examined; blood, cecum content, colon and brain were collected to evaluate metabolic parameters, endotoxin, gut microbiota, colon, and brain pathology.Results: We reported that acute L. edodes β-glucan supplementation prevented the gut microbial composition shift induced by the HF diet. Chronic L. edodes β-glucan supplementation prevented the HF diet-induced recognition memory impairment assessed by behavioral tests (the temporal order memory, novel object recognition and Y-maze tests). In the prefrontal cortex and hippocampus, the β-glucan supplementation ameliorated the alteration of synaptic ultrastructure, neuroinflammation and brain-derived neurotrophic factor (BDNF) deficits induced by HF diet. Furthermore, the β-glucan supplementation increased the mucosal thickness, upregulated the expression of tight junction protein occludin, decreased the plasma LPS level, and inhibited the proinflammatory macrophage accumulation in the colon of mice fed by HF diet. Conclusions: This study revealed that L. edodes β-glucan prevents cognitive impairments induced by the HF diet, which may occur via colon-brain axis improvement. The finding suggested that dietary L. edodes β-glucan supplementation may be an effective nutritional strategy to prevent obesity-associated cognitive decline.

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Silibinin rescues learning and memory deficits by attenuating microglia activation and preventing neuroinflammatory reactions in SAMP8 mice

Cited by 53 publications

References 27 publications

NLRP3 inflammasome activation contributes to long-term behavioral alterations in mice injected with lipopolysaccharide

NLRP3 inflammasome activation contributes to long-term behavioral alterations in mice injected with lipopolysaccharide

Curdlan Prevents the Cognitive Deficits Induced by a High-Fat Diet in Mice via the Gut-Brain Axis

β-glucan from Lentinula Edodes Prevents Cognitive Impairments in High-Fat Diet-Induced Obese Mice: Involvement of Colon-Brain Xxis

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Silibinin rescues learning and memory deficits by attenuating microglia activation and preventing neuroinflammatory reactions in SAMP8 mice

Cited by 53 publications

References 27 publications

NLRP3 inflammasome activation contributes to long-term behavioral alterations in mice injected with lipopolysaccharide

NLRP3 inflammasome activation contributes to long-term behavioral alterations in mice injected with lipopolysaccharide

Curdlan Prevents the Cognitive Deficits Induced by a High-Fat Diet in Mice via the Gut-Brain Axis

β-glucan from Lentinula Edodes Prevents&nbsp;Cognitive Impairments in&nbsp;High-Fat Diet-Induced Obese Mice: Involvement of Colon-Brain Xxis

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β-glucan from Lentinula Edodes Prevents Cognitive Impairments in High-Fat Diet-Induced Obese Mice: Involvement of Colon-Brain Xxis