Cattle Encephalon Glycoside and Ignotin Protects Neurons Against Microglia-Induced Neuroinflammation via Elevating BDNF
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ORIGINAL PAPER
Cattle Encephalon Glycoside and Ignotin Protects Neurons Against Microglia‑Induced Neuroinflammation via Elevating BDNF Expression and Inhibiting TLR4/NF‑κB Pathway Ya Gao1 · Jian Zhang1 · Shuyue Li1 · Yidan Zhang1 · Yuan Zhao1 · Cui Chang1 · Ya Qiu2 · Guofeng Yang1 Received: 20 July 2020 / Revised: 27 October 2020 / Accepted: 5 November 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Neuroinflammation is involved in the pathology and progression of Alzheimer’s disease (AD) and is closely related to microglial activation. We have previously reported that cattle encephalon glycoside and ignotin (CEGI) could inhibit the activation of microglia in APP/PS1 mice, a mouse model of familial AD. However, the anti-neuroinflammatory mechanisms of CEGI have not yet been fully elucidated. Here, we aimed to investigate the role of CEGI in microglia‐mediated neuroinflammation in AD. APP/PS1 mice were treated with CEGI intraperitoneally for 30 days, and then their cognition was assessed. We showed that CEGI alleviated cognitive damage with higher nesting scores, preferential indices, and spontaneous alternation rates in APP/PS1 mice. Moreover, CEGI treatment effectively reduced microglial activation and Iba-1 levels in the cortex of APP/PS1 mice. Additionally, CEGI decreased pro-inflammatory factors production and neuroinflammation-mediated neuronal damage in vivo and in vitro. Finally, CEGI upregulated BDNF levels and downregulated TLR4 and p-NF-κB p65 levels in vivo and in vitro. Taken together, these findings indicated that CEGI could attenuate cognitive deficits in APP/PS1 mice and suppress microglia‐induced neuroinflammation via increasing BDNF expression and inhibiting the TLR4/NF‐κB pathway. Keywords CEGI · Alzheimer’s disease · Microglia · Neuroinflammatory · Neuroprotection
Introduction Neuroinflammation is reportedly involved in the pathology and progression of Alzheimer’s disease (AD) [1]. Neuroinflammation observed in AD is characterized by the presence of activated microglia around the β‐amyloid (Aβ) deposits [2]. Activated microglia promote the release Ya Gao and Jian Zhang have equal responsibility as first author. * Ya Qiu [email protected] * Guofeng Yang [email protected] 1
Department of Geriatrics, Second Hospital of Hebei Medical University, Shijiazhuang 05000, Hebei, China
Institute of Geriatrics, 2nd Medical Center, Beijing Key Laboratory of Aging and Geriatrics, National Clinical Research Center of Geriatric Disease, Chinese PLA General Hospital & Chinese PLA Medical Academy, Beijing 100853, China
2
of pro-inflammatory factors, including interleukin (IL)‐1β, IL-6, and tumor necrosis factor (TNF)‐α, which cause neuronal damage and eventually cognitive deficits [3]. Therefore, intervention at the stage of microglial activation could help prevent neuronal damage from neuroinflammation and offer an alternative therapeutic strategy for AD [4–6]. Cattle encephalon glycoside and ignotin (CEGI) injection has been widely used in the treatment of acute ce
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