Naoling decoction restores cognitive function by inhibiting the neuroinflammatory network in a rat model of Alzheimer’s disease
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Zian Xia1,2,*, Weijun Peng1,*, Shunhua Cheng1,3, Bingwu Zhong1, Chenxia Sheng1, Chunhu Zhang2, Wei Gong1,4, Shuai Cheng1, Jun Li5 and Zhe Wang1
1Department of Integrated Traditional Chinese and Western Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China
2Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China
3Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China
4Department of Neurology, Liuyang Hospital of Traditional Chinese Medicine, Liuyang, Hunan 4103002, China
5Thyroid Tumour Internal Medicine Department, Cancer Hospital Affiliated to Xiangya School of Medicine, Central South University, Changsha 410013 Hunan, China
*These authors have contributed equally to this work
Zhe Wang, email: email@example.com
Keywords: Alzheimer’s disease, Naoling decoction, amyloid-beta (Aβ) deposits, neuroinflammatory network, Chromogranin A
Received: December 02, 2016 Accepted: April 10, 2017 Published: April 21, 2017
Neuroinflammation is central to the pathogenesis of Alzheimer’s disease (AD). We previously showed that Naoling decoction (NLD), a traditional Chinese medicine, was effective against AD, acting by inhibiting expression of IL-1β and IL-6. In the present study, we generated the rat model of AD by injecting Aβ1–42 peptide intracerebroventricularly and evaluated the dose-dependent effects of NLD treatment. The NLD-treated rats exhibited significant improvements in cognitive function as evaluated by the Morris water maze test. Golgi-Cox staining revealed that NLD treatment dose-dependently increased dendritic spines in the CA1 region, which were diminished in vehicle-treated rats. Further, NLD treatment normalized hippocampal Chromogranin A levels, which were elevated by Aβ1-42 induction. NLD also attenuated activation of microglia and astrocytes induced by Aβ1-42. Subsequently, NLD dose-dependently reduced levels TNF-α, IL-1β and IL-6 by inhibiting the NF-κB signaling pathway and the ASC-dependent inflammasome in the hippocampus. These findings reveal that NLD is a promising therapeutic agent that exerts inhibitory effects at multiple sites within the neuroinflammatory network induced in AD.
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