Cirsium japonicum var. Maackii Improves Cognitive Impairment under Amyloid Beta25-35-Induced Alzheimer’s Disease Model

Abstract

Abnormal production and degradation of amyloid beta (Aβ) in the brain lead to oxidative stress and cognitive impairment in Alzheimer’s disease (AD). Cirsium japonicum var. maackii (CJM) is widely used as an herbal medicine and has antibacterial and anti-inflammatory properties. This study focused on the protective effect of the ethyl acetate fraction from CJM (ECJM) on Aβ25-35-induced control mice. In the T-maze and novel object recognition test, ECJM provided higher spatial memory and object recognition compared to Aβ25-35 treatment alone. In the Morris water maze test, ECJM-administered mice showed greater learning and memory abilities than Aβ25-35-induced control mice. Additionally, ECJM-administered mice experienced inhibited lipid peroxidation and nitric oxide production in a dose-dependent manner. The present study indicates that ECJM improves cognitive impairment by inhibiting oxidative stress in Aβ25-35-induced mice. Therefore, CJM may be useful for the treatment of AD and may be a potential material for functional foods.

Literature review on the interdisciplinary biomarkers of multi-target and multi-time herbal medicine therapy to modulate peripheral systems in cognitive impairment

“…Therefore, a study on the therapeutic effect mechanism of HM via the peripheral system approach for cognitive impairment is needed. Research on the therapeutic effect and mechanism of HM in cognitive impairment animal models showed ameliorated cognitive deficits by anti-oxidation and anti-inflammation ( Huang et al, 2020 ; Gu et al, 2021 ; Pang et al, 2022 ). Additionally, treatment using YGY extract significantly mitigated cognitive deficits in a chronic renal failure mice model by up-regulating the CaMKIIα/CREBBDNF and EPO/EPOR pathways in the hippocampus ( Tang et al, 2019 ).…”

“…The oral administration of Danggui-Shaoyao-San (DSS) extract, which plays a positive effect in the up-regulation of DHA content in APPwse/PS1dE9 double transgenic mice, ameliorated cognitive deficits by anti-oxidation and anti-inflammation ( Huang et al, 2020 ). Pang et al (2022) reported that the oral administration of ethyl acetate fraction from Cirsium japonicum var. maackii (ECJM) inhibited lipid peroxidation and nitric oxide production in Aβ25-35-induced mice ( Pang et al, 2022 ).…”

“… Pang et al (2022) reported that the oral administration of ethyl acetate fraction from Cirsium japonicum var. maackii (ECJM) inhibited lipid peroxidation and nitric oxide production in Aβ25-35-induced mice ( Pang et al, 2022 ). Resveratrol oligomer, the seed coat extracts of Paeonia suffruticosa , treatments improved cognitive dysfunction in scopolamine-induced cognitive deficits in mice by inhibiting various biochemical markers, including cholinergic damage (acetyl choline esterase, choline acetyltransferase, and acetylcholine), oxidative (superoxide dismutase, catalase and glutathione) damage, and inflammatory (interleukins and tumor necrosis factor-α) pathways ( Liu et al, 2020 ).…”

Plant-Derived Bioactive Compounds in the Management of Neurodegenerative Disorders: Challenges, Future Directions and Molecular Mechanisms Involved in Neuroprotection

“…In a recent study, an ethyl-acetate fraction from the plant demonstrated neuroprotective effects, evidenced by improved spatial memory and object recognition in comparison to the untreated group. They also demonstrated a dose-dependent reduction in lipid peroxidation and NO generation, resulting in better cognitive impairment and antioxidant status in Aβ 25–35 -induced rats [ 101 ]. Of note, curcumin and resveratrol treatment showed decreased oxidative stress by inhibiting ROS generation, suppressed hyperphosphorylation of tau protein at threonine (T) 181 and T205, and protected SH-SY5Y cells from AβO damage [ 102 ].…”

Oxyresveratrol-β-cyclodextrin mitigates intracerebral STZ-induced Alzheimer’s disease via suppression of hippocampal and cortical cognitive impairment and histone deacetylase activity in rats: In silico and In vivo studies

“…It is the Aβ and the NFTs that are etiologically known responsible for the accompanying neuronal loss, cholinergic aberration, oxidative in ammation, and synaptic dysfunction. Thus, therapeutic approaches targeting mechanistic reduction of neuronal deposits of Aβ and NFTs have attracted attention (Pang et al 2022) nevertheless, there is no effective treatment or cure for AD currently.…”