Tetrandrine attenuates spatial memory impairment and hippocampal neuroinflammation via inhibiting NF-κB activation in a rat model of Alzheimer's disease induced by amyloid-β(1–42)

He, Fu‐Qian; Qiu, Bo-yun; Zhang, Xiao-Hui; Li, Tianke; Xie, Quan; Cui, Dejun; Huang, Xiaoli; Gan, Hui-Li

doi:10.1016/j.brainres.2011.01.103

Cited by 103 publications

(55 citation statements)

References 43 publications

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“…Generation and amplification of TNF-a and IL-1b have been reported to be regulated by NF-jB p65 [26][27][28]. In addition to NF-jB p65 signaling, MAPKs are also important signaling molecules involved in the production of pro-inflammatory mediators and cytokines and the modulation of NF-jB p65 in microglia [29,30].…”

Section: Discussionmentioning

confidence: 99%

Neochlorogenic Acid Inhibits Lipopolysaccharide-Induced Activation and Pro-inflammatory Responses in BV2 Microglial Cells

et al. 2015

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Microglia is the resident innate immune cells that sense pathogens and tissue injury in the central nervous system. Microglia becomes activated in response to injury, infection, and other stimuli that threaten neuronal survival. Microglia activation plays an important role in neurodegenerative diseases. Neochlorogenic acid (NCA) is a natural polyphenolic compound found in dried fruits and other plants. Although previous studies have shown that phenolic acids including NCA have outstanding antioxidant, antibacterial, antiviral, and antipyretic activities, there has not yet been investigated for anti-inflammatory effects. Therefore, for the first time we have examined the potential of NCA to inhibit microglial activation and pro-inflammatory responses in the brain. We found that lipopolysaccharide-induced inducible nitric oxide synthase, and cyclooxygenase-2 expression, and nitric oxide formation was suppressed by NCA in a dose-dependent manner in BV2 microglia. NCA also inhibited the production of pro-inflammatory mediators, tumor necrosis factor-α and interleukin-1 beta. Furthermore, phosphorylated nuclear factor-kappa B p65 and p38 mitogen-activated protein kinase activation were blocked by NCA. Taken together, these results suggest that NCA exerts neuroprotective effects through the inhibition of pro-inflammatory pathways in activated microglia.

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Section: Discussionmentioning

confidence: 99%

Neochlorogenic Acid Inhibits Lipopolysaccharide-Induced Activation and Pro-inflammatory Responses in BV2 Microglial Cells

et al. 2015

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“…In fact, activated NF-κB has been demonstrated in microglia and astrocytes of patients with AD [11]. Studies have also shown that NF-κB activation accompanied by secretion of the proinflammatory cytokines is associated with neuronal degeneration in the brains of patients with AD [12,13].…”

Section: Introductionmentioning

confidence: 95%

Lycopene abrogates Aβ(1–42)-mediated neuroinflammatory cascade in an experimental model of Alzheimer’s disease

Sachdeva

Chopra

2015

The Journal of Nutritional Biochemistry

163

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“…NF-kB signaling activated by RAGE could induce many inflammatory pathways and increase expression of cell-associated RAGE (Lue et al 2001). Activation of RAGE/NF-jB signaling pathway leads to neuronal oxidative stress and neuroinflammation (Fang et al 2010;He et al 2011), on the contrary, inhibition of RAGE/NF-jB signaling pathway protects against AD (Chen et al 2007). Thus, Akt/ Nrf2 and RAGE/NF-jB signaling pathways has been considered as potential therapeutic targets for AD (Tan et al 2015).…”

Section: Introductionmentioning

confidence: 98%

Hesperidin attenuates learning and memory deficits in APP/PS1 mice through activation of Akt/Nrf2 signaling and inhibition of RAGE/NF-κB signaling

Hong

2015

Arch. Pharm. Res.

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Numerous studies have demonstrated that oxidative stress and inflammation play a pivotal role in the pathophysiology of Alzheimer disease (AD). Hesperidin (HP) has various pharmacological effects including anti-oxidative, anti-inflammatory and neuroprotective properties. In this study, APP/PS1 mice were used to evaluate the neuroprotective effects of HP. We reported that intragastric administration of HP (40 mg/kg) for 90 days significantly attenuated cognitive impairment in APP/PS1 mice. HP treatment suppressed oxidative stress by reducing the levels of ROS, LPO, protein carbonyl and 8-OHdG and increasing the activity of HO-1, SOD, catalase, and GSH-Px. HP treatment also inhibited inflammation by decreasing the levels of TNF-α, C-reactive protein and MCP-1 and reducing the activity of NF-κB. Moreover, HP could reverse the decreased phosphorylation of Akt, the decreased phosphorylation of GSK-3β, the lessened Nrf2 and the reduced expression of HO-1. HP could also inhibit the increased the RAGE expression, the enhanced phosphorylation of IκBα, and the augmented nuclear translocation of NF-κB/p65 in cortex of APP/PS1 mice. Taken together, HP suppresses oxidative stress and inflammation via activation of Akt/Nrf2 signaling and inhibition of RAGE/NF-κB signaling and further confers neuroprotection.

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Tetrandrine attenuates spatial memory impairment and hippocampal neuroinflammation via inhibiting NF-κB activation in a rat model of Alzheimer's disease induced by amyloid-β(1–42)

Cited by 103 publications

References 43 publications

Neochlorogenic Acid Inhibits Lipopolysaccharide-Induced Activation and Pro-inflammatory Responses in BV2 Microglial Cells

Neochlorogenic Acid Inhibits Lipopolysaccharide-Induced Activation and Pro-inflammatory Responses in BV2 Microglial Cells

Lycopene abrogates Aβ(1–42)-mediated neuroinflammatory cascade in an experimental model of Alzheimer’s disease

Hesperidin attenuates learning and memory deficits in APP/PS1 mice through activation of Akt/Nrf2 signaling and inhibition of RAGE/NF-κB signaling

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