Curcumin inhibits Aβ-induced microglial inflammatory responses in vitro: Involvement of ERK1/2 and p38 signaling pathways

Shi, Xiaolei; Zheng, Zhaomin; Li, Jie; Xiao, Zijian; Qi, Weiwei; Zhang, Aiwu; Wu, Qi; Yu, Fang

doi:10.1016/j.neulet.2015.03.045

Cited by 97 publications

(52 citation statements)

References 22 publications

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“…Mouse microglia were isolated from the brains using a modification of the procedure XU ET AL. | 905 described in our previous study (Shi et al, 2015). Briefly, the brains were immediately dissociated in ice-cold PBS.…”

Section: Primary Microglia Culture and MCMmentioning

confidence: 99%

MFG‐E8 reverses microglial‐induced neurotoxic astrocyte (A1) via NF‐κB and PI3K‐Akt pathways

Zhang

Zhu

et al. 2018

Journal Cellular Physiology

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143

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Recent evidence have suggested that neuroinflammation and ischemia induce the activation of two different types of reactive astrocytes, termed A1 and A2. Additionally, A1 astrocytes contribute to the death of neurons and oligodendrocytes in neurodegenerative diseases, such as Alzheimer's disease (AD). In the current study, we constructed an Aβ42-activated microglia-conditioned medium to induce A1 astrocytic activation via secretion of interleukin 1α, tumor necrosis factor, and complement component 1q in vitro, and indicated the regulatory role of milk fat globule epidermal growth factor 8 (MFG-E8) on A1/A2 astrocytic alteration through the downregulation of nuclear factor-κB and the upregulation of PI3K-Akt. This study showed that MFG-E8 suppressed A1 astrocytes and holds great potential for the treatment of AD.

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Section: Primary Microglia Culture and MCMmentioning

confidence: 99%

MFG‐E8 reverses microglial‐induced neurotoxic astrocyte (A1) via NF‐κB and PI3K‐Akt pathways

Zhang

Zhu

et al. 2018

Journal Cellular Physiology

Self Cite

143

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“…Curcumin 0.01-10 µM for 1 hr Mouse primary microglia exposed to Aβ42 Protected microglia against Aβ42 by inhibiting Aβstimulated MAPKs signaling pathways X. Shi et al (2015) Curcumin 10 μM for 24 hr Primary hippocampus neuronal/glial from the brain of rat embryos exposed to Aβ Reduced the activation of microglia and astrocytes, as well as cytokine production and inhibited NF-κB signaling pathway Liu et al (2016) Curcumin 5 μg/ml for 30 min HT22 murine hippocampal neuronal cells exposed to acrolein Prevented AD-like pathologies by increasing the levels of GSH and SOD, and decreasing MDA level, A-disintegrin, metalloprotease and also amyloid precursor protein, βsecretase, and receptor for advanced glycation end products modulating the BDNF/TrkB signaling L. Y. Shi et al (2018) Curcumin 66.3 µM for 24 hr SH-SY5Y cells exposed Aβ Ameliorated AD-like pathology by modulating mitochondrial function, dynamics, biogenesis and synaptic activity Reddy et al (2016) Di-O-demethylcurcumin 1,2,4,8 µM for 2 hr SK-N-SH cells exposed to Aβ25-35 Improved cell viability.…”

Section: Referencesmentioning

confidence: 99%

The impact of curcumin and its modified formulations on Alzheimer's disease

Farkhondeh

Samarghandian

Pourbagher‐Shahri

et al. 2019

Journal Cellular Physiology

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Alzheimer's disease (AD) is a major health problem worldwide, with no effective treatment approach. Curcumin is the main ingredient of turmeric traditionally used in Asian medicine. Several experimental studies have indicated the protective effect of curcumin and its novel formulations in AD. Curcumin has antioxidant, anti‐inflammatory and neurotrophic activities, proposing a strong potential to prevent neurodegenerative diseases. However, there are no sufficient clinical trials to confirm curcumin use in AD patients. Low bioavailability following oral administration of curcumin limits its usage in human. The present study was designed to gather the effects of curcumin and its modified formulations in human and experimental models of AD.

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“…Galangal extract showed anti‐amnesic effects in AD‐like mice, induced by amyloid‐beta toxicity (Hanish Singh et al ., ). Ginger and turmeric extracts and their constituents have been shown to have neuroprotective effects in several neurodegenerative disease models, including AD (Azam et al ., ; Garcia‐Alloza et al ., ; Moon et al ., ; Shi et al ., ; Zeng et al ., ). In addition, turmeric improved cognition by upregulating neurotrophic factors and CREB signaling (Nam et al ., ).…”

Section: Resultsmentioning

confidence: 97%

Effects of Myoga on Memory and Synaptic Plasticity by Regulating Nerve Growth Factor-Mediated Signaling

Kim

Lim

et al. 2015

Phytother. Res.

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The flower bud of Zingiber mioga Roscoe, known as 'myoga' or Japanese ginger, has a pungent aroma and is commonly consumed as a spice, with pickles, or as a health supplement in Eastern Asia. Here, we evaluated the activity of myoga in the brain, focusing especially on nerve growth factor (NGF), which is believed to mediate synaptic plasticity, supporting learning and memory. In a rat primary hippocampal astrocyte culture system, treatment with myoga extract for 24 h significantly stimulated the production of NGF. In mice administered myoga extract for 14 days, 200 and 400 mg/kg/day treatment resulted in increased NGF levels in the hippocampus. Myoga extract treatment also regulated the phosphorylation of extracellular signal-regulated kinases and cAMP response element-binding protein in the mouse hippocampus, leading to increased synaptic plasticity. In addition, it significantly increased novel object recognition time and spontaneous alternation, indicating improvement in learning and memory. These results suggest that myoga helps regulate NGF and synaptic plasticity, increasing memory ability.

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Curcumin inhibits Aβ-induced microglial inflammatory responses in vitro: Involvement of ERK1/2 and p38 signaling pathways

Cited by 97 publications

References 22 publications

MFG‐E8 reverses microglial‐induced neurotoxic astrocyte (A1) via NF‐κB and PI3K‐Akt pathways

MFG‐E8 reverses microglial‐induced neurotoxic astrocyte (A1) via NF‐κB and PI3K‐Akt pathways

The impact of curcumin and its modified formulations on Alzheimer's disease

Effects of Myoga on Memory and Synaptic Plasticity by Regulating Nerve Growth Factor-Mediated Signaling

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