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Publication : Formulated Chinese medicine Shaoyao Gancao Tang reduces NLRP1 and NLRP3 in Alzheimer's disease cell and mouse models for neuroprotection and cognitive improvement.

First Author  Chiu YJ Year  2021
Journal  Aging (Albany NY) Volume  13
Issue  11 Pages  15620-15637
PubMed ID  34106880 Mgi Jnum  J:368890
Mgi Id  MGI:8215673 Doi  10.18632/aging.203125
Citation  Chiu YJ, et al. (2021) Formulated Chinese medicine Shaoyao Gancao Tang reduces NLRP1 and NLRP3 in Alzheimer's disease cell and mouse models for neuroprotection and cognitive improvement. Aging (Albany NY) 13(11):15620-15637
abstractText  Amyloid beta (Abeta) plays a major role in the neurodegeneration of Alzheimer's disease (AD). The accumulation of misfolded Abeta causes oxidative stress and inflammatory damage leading to apoptotic cell death. Traditional Chinese herbal medicine (CHM) has been widely used in treating neurodegenerative diseases by reducing oxidative stress and neuroinflammation. We examined the neuroprotective effect of formulated CHM Shaoyao Gancao Tang (SG-Tang, made of Paeonia lactiflora and Glycyrrhiza uralensis at 1:1 ratio) in AD cell and mouse models. In Abeta-GFP SH-SY5Y cells, SG-Tang reduced Abeta aggregation and reactive oxygen species (ROS) production, as well as improved neurite outgrowth. When the Abeta-GFP-expressing cells were stimulated with conditioned medium from interferon (IFN)-gamma-activated HMC3 microglia, SG-Tang suppressed expressions of inducible nitric oxide synthase (iNOS), NLR family pyrin domain containing 1 (NLRP1) and 3 (NLRP3), tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-6, attenuated caspase-1 activity and ROS production, and promoted neurite outgrowth. In streptozocin-induced hyperglycemic APP/PS1/Tau triple transgenic (3xTg-AD) mice, SG-Tang also reduced expressions of NLRP1, NLRP3, Abeta and Tau in hippocampus and cortex, as well as improved working and spatial memories in Y maze and Morris water maze. Collectively, our results demonstrate the potential of SG-Tang in treating AD by moderating neuroinflammation.
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