Diammonium Glycyrrhizinate Attenuates Aβ 1–42 ‐Induced Neuroinflammation and Regulates MAPK and NF‐κB Pathways In Vitro and In Vivo-Reference-Cited by-同舟云学术

Diammonium Glycyrrhizinate Attenuates Aβ 1–42 ‐Induced Neuroinflammation and Regulates MAPK and NF‐κB Pathways In Vitro and In Vivo

Published:2012-12-20 Issue:2 Volume:19 Page:117-124
ISSN:1755-5930
Container-title:CNS Neuroscience & Therapeutics
language:en
Short-container-title:CNS Neurosci Ther

Author:

Zhao Hui¹²,Wang Su‐Lei¹,Qian Lai²,Jin Jia‐Li²,Li Hui¹,Xu Yun¹²³⁴,Zhu Xiao‐Lei¹²³

Affiliation:

1. Department of Neurology Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine Nanjing University of Chinese Medicine Nanjing China

2. Department of Neurology Affiliated Drum Tower Hospital of Nanjing University Medical School Nanjing China

3. The State Key Laboratory of Pharmaceutical Biotechnology Nanjing University Nanjing China

4. Jiangsu Key Laboratory for Molecular Medicine Nanjing China

Funder

National Nature Science Foundation of China

State Key Laboratory of Pharmaceutical Biotechnology of Nanjing University

Medical Leading Talent and Innovation Team Project of Jiangsu Province

National Natural Science Foundation of Jiangsu Province of China

Key Project of Nanjing Municipal Bureau of Health

Publisher

Wiley

Subject

Pharmacology (medical),Physiology (medical),Psychiatry and Mental health,Pharmacology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/cns.12043

Reference27 articles.

1. Neurodegenerative disease and adult neurogenesis

2. The potential role of proinflammatory and antiinflammatory cytokines in Alzheimer disease pathogenesis

3. 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)

4. A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines

5. A novel p38α MAPK inhibitor suppresses brain proinflammatory cytokine up-regulation and attenuates synaptic dysfunction and behavioral deficits in an Alzheimer's disease mouse model

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