机构：[1]Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing, P.R. China.神经科系统神经内科首都医科大学宣武医院神经疾病高创中心（北京学者工作室）[2]Beijing Key Laboratory of Geriatric Cognitive Disorders, Beijing, P.R. China.[3]Clinical Center for Neurodegenerative Disease and Memory Impairment, Capital Medical University, Beijing, P.R. China.[4]Center of Alzheimer's Disease, Beijing Institute for Brain Disorders, Beijing, P.R. China.
Inflammation and oxidative stress are believed to play an important role in the pathogenesis of Alzheimer's disease (AD). Tenuifolin (TEN) is a natural neuroprotective compound extracted from Polygala tenuifolia Willd, which may improve cognitive symptoms.
This study was designed to evaluate the protective effect of TEN on inflammatory and oxidative stress induced by amyloid-β (Aβ)42 oligomers in BV2 cells, and to explore the underlying mechanisms.
We conducted cell viability assays to estimate drug toxicity and drug effects on cells. Quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assays were performed to detect the release of inflammatory factors. Nitric oxide (NO) assays were used to measure the degree of oxidative stress. Western blot and immunofluorescence analysis were used to explore the influence of TEN on the nuclear factor-κB (NF-κB) pathway.
Pretreatment of BV2 microglial cells with TEN inhibited the release of tumor necrosis factor-α, interleukin-6, and interleukin-1β, alleviated NO-induced oxidative stress by inhibiting the expression of inducible nitric oxide synthase and cyclo-oxygenase-2, and protected SH-SY5Y cells from the toxicity induced by the medium conditioned by BV2 cells previously exposed to Aβ42 oligomers. Moreover, TEN suppressed upstream activators of NF-κB, as well as NF-κB translocation to the nucleus in BV2 microglial cells.
This study demonstrates that TEN can protect SH-SY5Y cells from Aβ42 oligomer-induced microglia-mediated inflammation, and oxidative stress by downregulating the NF-κB signaling pathway.
基金：
This study was supported by the Key Project
of the National Natural Science Foundation of
China (81530036); the National Key Scientific
Instrument and Equipment Development Project
(31627803); Mission Program of Beijing Munici-
pal Administration of Hospitals (SML20150801);
Beijing Scholars Program; Beijing Brain Initiative
from Beijing Municipal Science & Technol-
ogy Commission (Z161100000216137); Project for
Outstanding Doctor with Combined Ability of
Western and Chinese Medicine; and Beijing Munic-
ipal Commission of Health and Family Planning
(PXM2019 026283 000003).
第一作者机构：[1]Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing, P.R. China.
通讯作者：
通讯机构：[*1]Department of Neurology, Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R.China.
推荐引用方式(GB/T 7714)：
Chen Shuoqi,Jia Jianping.Tenuifolin Attenuates Amyloid-β42-Induced Neuroinflammation in Microglia Through the NF-κB Signaling Pathway.[J].JOURNAL OF ALZHEIMERS DISEASE.2020,76(1):195-205.doi:10.3233/JAD-200077.
APA：
Chen Shuoqi&Jia Jianping.(2020).Tenuifolin Attenuates Amyloid-β42-Induced Neuroinflammation in Microglia Through the NF-κB Signaling Pathway..JOURNAL OF ALZHEIMERS DISEASE,76,(1)
MLA：
Chen Shuoqi,et al."Tenuifolin Attenuates Amyloid-β42-Induced Neuroinflammation in Microglia Through the NF-κB Signaling Pathway.".JOURNAL OF ALZHEIMERS DISEASE 76..1(2020):195-205
