1. Korean Red Pine ( Pinus densiflora ) Bark Extract Attenuates Aβ-Induced Cognitive Impairment by Regulating Cholinergic Dysfunction and Neuroinflammation.
- Author
-
Go MJ, Kim JM, Kang JY, Park SK, Lee CJ, Kim MJ, Lee HR, Kim TY, Joo SG, Kim DO, and Heo HJ
- Subjects
- Acetylcholine metabolism, Acetylcholine pharmacology, Acetylcholinesterase metabolism, Adenosine Triphosphate metabolism, Amyloid beta-Peptides, Animals, Antioxidants pharmacology, Brain-Derived Neurotrophic Factor metabolism, Choline O-Acetyltransferase metabolism, Choline O-Acetyltransferase pharmacology, Cholinergic Agents pharmacology, Glutathione metabolism, Malondialdehyde metabolism, Malondialdehyde pharmacology, Mice, NF-KappaB Inhibitor alpha metabolism, Neuroinflammatory Diseases, Oxidative Stress, Plant Bark, Plant Extracts pharmacology, Reactive Oxygen Species metabolism, Republic of Korea, Superoxide Dismutase metabolism, Synaptophysin metabolism, Synaptophysin pharmacology, Tumor Necrosis Factor-alpha metabolism, bcl-2-Associated X Protein metabolism, Cognitive Dysfunction chemically induced, Cognitive Dysfunction drug therapy, Neuroprotective Agents pharmacology, Pinus
- Abstract
In this study, we investigated the anti-amnesic effect of Korean red pine ( Pinus densiflora ) bark extract (KRPBE) against amyloid beta
1-42 (Aβ1-42 )-induced neurotoxicity. We found that treatment with KRPBE improved the behavioral function in Aβ-induced mice, and also boosted the antioxidant system in mice by decreasing malondialdehyde (MDA) content, increasing superoxide dismutase (SOD) activities, and reducing glutathione (GSH) levels. In addition, KRPBE improved the cholinergic system by suppressing reduced acetylcholine (ACh) content while also activating acetylcholinesterase (AChE), regulating the expression of choline acetyltransferase (ChAT), postsynaptic density protein-95 (PSD-95), and synaptophysin. KRPBE also showed an ameliorating effect on cerebral mitochondrial deficit by regulating reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and ATP levels. Moreover, KRPBE modulated the expression levels of neurotoxicity indicators Aβ and phosphorylated tau (p-tau) and inflammatory cytokines TNF-α, p-IκB-α, and IL-1β. Furthermore, we found that KRPBE improved the expression levels of neuronal apoptosis-related markers BAX and BCl-2 and increased the expression levels of BDNF and p-CREB. Therefore, this study suggests that KRPBE treatment has an anti-amnestic effect by modulating cholinergic system dysfunction and neuroinflammation in Aβ1-42 -induced cognitive impairment in mice.- Published
- 2022
- Full Text
- View/download PDF