Bee venom ameliorates lipopolysaccharide-induced memory loss by preventing NF-kappaB pathway

Gu, Sun Mi; Park, Mi Hee; Hwang, Chul Ju; Song, Ho Sueb; Lee, Ung Soo; Han, Sang Bae; Oh, Ki Wan; Ham, Young Wan; Song, Min Jong; Son, Dong Ju; Hong, Jin Tae

doi:10.1186/s12974-015-0344-2

Cited by 55 publications

(66 citation statements)

References 60 publications

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“…Collectively, this highlights the crucial role of S100B in AD onset and progression and the relevant effects of IL-17Abs in reducing its expression in mouse whole brain. During the confirmation of the inhibition of the inflammatory state with IL-17 neutralizing antibodies, we also observed, using immunofluorescence techniques, that expression of GFAP and Iba-1 (as indices of astrocytes and microglia activation; Gu et al, 2015;Liddelow et al, 2017) was markedly reduced after IL-17 Abs treatments.…”

Section: Discussionmentioning

confidence: 67%

Neutralization of IL‐17 rescues amyloid‐β‐induced neuroinflammation and memory impairment

Cristiano

Volpicelli

Lippiello

et al. 2019

British J Pharmacology

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Background and purpose Alzheimer's disease (AD) is a common neurodegenerative disease characterized by a neuroinflammatory state, and to date, there is no cure and its treatment represents a large unmet clinical need. The involvement of Th17 cells in the pathogenesis of AD‐related neuroinflammation has been reported in several studies. However, the role of the cytokine, IL‐17 has not been well addressed. Herein, we investigate the effects of IL‐17 neutralizing antibody (IL‐17Ab) injected by i.c.v. or intranasal (IN) routes on amyloid‐β (Aβ)‐induced neuroinflammation and memory impairment in mice. Experimental approach Aβ1–42 was injected into cerebral ventricles of adult CD1 mice. These mice received IL‐17Ab via i.c.v. either at 1 h prior to Aβ1–42 injection or IN 5 and 12 days after Aβ1–42 injection. After 7 and 14 days of Aβ1–42 administration, we evaluated olfactory, spatial and working memory and performed biochemical analyses on whole brain and specific brain areas. Key results Pretreatment with IL‐17Ab, given, i.c.v., markedly reduced Aβ1–42‐induced neurodegeneration, improved memory function, and prevented the increase of pro‐inflammatory mediators in a dose‐dependent manner at 7 and 14 days. Similarly, the double IN administration of IL‐17Ab after Aβ1–42 injection reduced neurodegeneration, memory decline, and the levels of proinflammatory mediators and cytokines. Conclusion and implications These findings suggest that the IL‐17Ab reduced neuroinflammation and behavioural symptoms induced by Aβ. The efficacy of IL‐17Ab IN administration in reducing Aβ1–42 neurodegeneration points to a possible future therapeutic approach in patients with AD. Linked Articles This article is part of a themed section on Therapeutics for Dementia and Alzheimer's Disease: New Directions for Precision Medicine. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.18/issuetoc

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Section: Discussionmentioning

confidence: 67%

Neutralization of IL‐17 rescues amyloid‐β‐induced neuroinflammation and memory impairment

Cristiano

Volpicelli

Lippiello

et al. 2019

British J Pharmacology

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“…A spatial memory test was performed as previously described, with minor modifications (10). The Morris water maze is a white circular pool (150 cm in diameter and 35 cm high) with a fea‐tureless inner surface (Shanghai Xinruan Information Technol‐ogy).…”

Section: Methodsmentioning

confidence: 99%

“…It also stimulates β‐secretase 1 (BACE1) transcription, which subsequently decomposes APP and leads to the generation of Aβ (9). Numerous reports in the literature have also demonstrated that an intraperitoneal injection of LPS impairs memory performance and enhances amyloidogenesis via stimulating the NF‐κB signaling pathway (10).…”

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confidence: 99%

Chicoric acid supplementation prevents systemic inflammation‐induced memory impairment and amyloidogenesis via inhibition of NF‐κB

et al. 2016

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Chicoric acid (CA), a natural phenolic acid extracted from chicory and the echinacea (purple coneflower) plant (), has been regarded as a nutraceutical that has powerful antioxidant and antiobesity activities. We investigated the inhibitory effects of CA on systemic inflammation-induced neuroinflammation, amyloidogenesis, and cognitive impairment. C57BL/6J mice were treated with 0.05% CA in the drinking water for 45 d. The mice were then treated by intraperitoneal injection of lipopolysaccharide (LPS). It was found that CA prevented LPS-induced memory impairment and neuronal loss through behavioral tests and histological examination. Furthermore, amyloidogenesis in the CNS was detected. The results showed that CA prevented LPS-induced increases in amyloid β (1-42 specific) (Aβ) accumulation, levels of amyloid precursor protein, and neuronal β-secretase 1 (BACE1), as well as the equilibrium cholinergic system in mouse brain. Moreover, CA down-regulated LPS-induced glial overactivation by inhibiting the MAPK and NF-κB pathway. Consequently, CA reduced the levels of NF-κB transcriptionally regulated inflammatory mediators and cytokines such as iNOS, cyclooxygenase-2 (COX-2), IL-1β, and TNF-α in both mouse brain and BV2 microglial cells. These results demonstrated that CA alleviated memory impairment and amyloidogenesis triggered by LPS through suppressing NF-κB transcriptional pathway, suggesting that CA might be a plausible therapeutic intervention for neuroinflammation-related diseases such as Alzheimer disease.-Liu, Q., Chen, Y., Shen, C., Xiao, Y., Wang, Y., Liu, Z., Liu, X. Chicoric acid supplementation prevents systemic inflammation-induced memory impairment and amyloidogenesis inhibition of NF-κB.

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“…Three-dimensional structure of Nrf2-DNA complexes was retrieved from protein data bank (PDB code: 2FLU) to be used for the present docking study [31]. Molecular docking studies mainly involve selection and preparation of appropriate protein, grid generation, ligand preparation followed by docking & its analysis.…”

Section: Molecular Docking and Mm-gbsa Binding Free Energymentioning

confidence: 99%

Rosuvastatin alleviates high-salt and cholesterol diet-induced cognitive impairment in rats via Nrf2–ARE pathway

et al. 2018

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Objective: The objectives of our study were to investigate the possible effect of rosuvastatin in ameliorating high salt and cholesterol diet (HSCD)-induced cognitive impairment and to also investigate its possible action via the Nrf2-ARE pathway. Methods: In silico studies were performed to check the theoretical binding of rosuvastatin to the Nrf2 target. HSCD was used to induce cognitive impairment in rats and neurobehavioral studies were performed to evaluate the efficacy of rosuvastatin in enhancing cognition. Biochemical analyses were used to estimate changes in oxidative markers. Western blot and immunohistochemical analyses were done to check Nrf2 translocation. TUNEL and caspase 3 tests were performed to evaluate reversal of apoptosis by rosuvastatin. Results: Rosuvastatin showed good theoretical affinity to Nrf2, significantly reversed changes in oxidative biomarkers which were induced by HSCD, and also improved the performance of rats in the neurobehavioral test. A rise in nuclear translocation of Nrf2 was revealed through immunohistochemical analysis and western blot. TUNEL staining and caspase 3 activity showed attenuation of apoptosis. Discussion: We have investigated a novel mechanism of action for rosuvastatin (via the Nrf2-ARE pathway) and demonstrated that it has the potential to be used in the treatment of cognitive impairment. KEYWORDSCognitive impairment; rosuvastatin; high-salt and cholesterol diet; oxidative stress; Nrf2; nuclear factor (erythroid-derived 2)-like 2

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Bee venom ameliorates lipopolysaccharide-induced memory loss by preventing NF-kappaB pathway

Cited by 55 publications

References 60 publications

Neutralization of IL‐17 rescues amyloid‐β‐induced neuroinflammation and memory impairment

Neutralization of IL‐17 rescues amyloid‐β‐induced neuroinflammation and memory impairment

Chicoric acid supplementation prevents systemic inflammation‐induced memory impairment and amyloidogenesis via inhibition of NF‐κB

Rosuvastatin alleviates high-salt and cholesterol diet-induced cognitive impairment in rats via Nrf2–ARE pathway

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