Green Tea Attenuates the Particulate Matter (PM)-Exposed Gut-Brain Axis Dysfunction through Regulation of Intestinal Microenvironment and Hormonal Changes.

Chronic exposure to particulate matter (PM)2.5 causes brain damage through intestinal imbalance. This study was estimated to confirm the regulatory activity of green tea against chronic PM exposure-induced abnormal gut-brain axis (GBA) in BALB/c mice.

Ameliorates Cognitive Impairment on Amyloid β-Induced Neurotoxicity by Modulating Oxidative Stress and Synaptic Function in Institute of Cancer Research (ICR) Mice.

This study investigated the neuroprotective effect of 70% ethanol extract of (EE) in amyloid beta (Aβ)-induced cognitive deficit mice. As a result of analyzing the bioactive compounds in EE, nine compounds were identified using ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS). In particular, the diekcol content was quantified by high-performance liquid chromatography with diode-array detection (DAD-HPLC).

Leaves Alleviate Cognitive Dysfunction in Dextran Sulfate Sodium (DSS)-Induced Colitis Mice through Regulating JNK/TLR4 Signaling Pathway.

Ulcerative colitis (UC) is one of the inflammatory bowel diseases (IBD) that is characterized by systemic immune system activation. This study was performed to assess the alleviative effect of administering an aqueous extract of leaves (AEEL) on cognitive dysfunction in mice with dextran sulfate sodium (DSS)-induced colitis. The major bioactive compounds of AEEL were identified as a quinic acid derivative, caffeic acid-O-hexoside, and 3-O-caffeoylquinic acid using UPLC Q-TOF/MS.

Hepatoprotective Effect of Extracts on Chronic Alcohol-Induced Fatty Liver and Hepatic Inflammation in C57BL/6 Mice.

This study was performed to investigate the protective effects of on fatty liver and hepatitis in chronic alcohol-induced hepatotoxicity. The physiological compounds of a mixture of aqueous and 60% ethanol (2:8, /) extracts of (EA) were identified as kestose, raffinose, kaempferol and quercetin glucoside, and kaempferol di-glucoside by UPLC Q-TOF MS. The EA regulated the levels of lipid metabolism-related biomarkers such as total cholesterol, triglyceride, low-density lipoprotein (LDL), and high-density lipoprotein (HDL)-cholesterol in serum.

Fermented Larvae Improves Neurotoxicity in Chronic Ethanol-Induced-Dementia Mice via Suppressing AKT and NF-κB Signaling Pathway.

This study was investigated to examine the neuroprotective effect of fermented larvae (FPB) in ethanol-induced-dementia mice. Consumption of FPB by mice resulted in improved memory dysfunction in the Y-maze, passive avoidance, and Morris water maze tests. FPB significantly decreased oxidative stress by regulating levels of malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) in brain tissues.

Fermented Larvae Ameliorates Chronic Ethanol-Induced Hepatotoxicity in Mice via AMPK and TLR-4/TGF-β1 Pathways.

This study evaluated the hepatoprotective effect of fermented larvae (FPB) in ethanol-induced liver injury mice. As a result of amino acids in FPB, 18 types of amino acids including essential amino acids were identified. In the results of in vitro tests, FPB increased alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) activities.

Anti-Amnesia-like Effect of Extract by Improving Apoptosis and Neuroinflammation on Trimethyltin-Induced ICR Mice.

This study was conducted to investigate the anti-amnestic property of Korean red pine bark extract (KRPBE) on TMT-induced cognitive decline in ICR mice. As a result of looking at behavioral function, the consumption of KRPBE improved the spatial work ability, short-term learning, and memory ability by Y-maze, passive avoidance, and Morris water maze tests. KRPBE suppressed antioxidant system damage by assessing the SOD activity, reduced GSH content, and MDA levels in brain tissue.

Suppressed Chronic PM-Exposed Pulmonary Dysfunction via TLR/TGF-β Pathway in BALB/c Mice.

This study investigated the ameliorating effect of the aqueous extract of on PM-induced pulmonary dysfunction. The major compounds of were identified as palmitic acid, stearic acid, and oleamide using GC/MS and hexadecanamide, oleamide, and 13-docosenamide using UPLC-Q-TOF/MS. improved pulmonary antioxidant system deficit by regulating SOD activities and reducing GSH levels and MDA contents.

Korean Red Ginseng Prevents the Deterioration of Lung and Brain Function in Chronic PM-Exposed Mice by Regulating Systemic Inflammation.

This study was conducted to confirm the effects of Korean red ginseng on lung and brain dysfunction in a BALB/c mice model exposed to particulate matter (PM) for 12 weeks. Learning and cognitive abilities were assessed with Y-maze, passive avoidance, and Morris water maze tests. To evaluate the ameliorating effect of red ginseng extract (RGE), the antioxidant system and mitochondrial function were investigated.

Suppresses PM-Induced Cognitive Dysfunction by Regulating Gut-Brain Axis via TLR-4/MyD88 Pathway.

This study was conducted to evaluate the cognitive dysfunction improvement effect of aqueous extract of (AECF) by regulating the imbalance of the gut-brain axis in chronic particulate matter (PM)-exposed mice. The physiological compounds of AECF were identified as hexadecanamide, oleamide, octadecanamide, stearidonic acid, and linolenic acid by the ultra-performance liquid chromatography-quadrupole time of flight mass spectrometry (UPLC Q-TOF MS) analysis. To evaluate the effect of PM on the antioxidant system, superoxide dismutase (SOD) contents, reduced glutathione (GSH) contents, and malondialdehyde (MDA) contents were measured in colon and brain tissues.

Protective Effect of on PM-Induced Pulmonary Damage in BALB/c Mice via the TGF-β and NF-κB Pathway.

This study aimed to assess the protective effect of an extract of against particulate-matter (PM)-induced pulmonary inflammation and fibrosis. The compounds with physiological activity were identified as shanzhiside, secologanoside, loganic acid, chlorogenic acid, secologanic acid, secoxyloganin, quercetin pentoside, and dicaffeoyl quinic acids (DCQA), including 3,4-DCQA, 3,5-DCQA, 4,5-DCQA, and 1,4-DCQA using ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS). The extract of reduced cell death, reactive oxygen species (ROS) production, and inflammation in A549 cells.

A Mixture of and Improves PM-Induced Cognitive Dysfunction by Regulating Oxidative Stress and Inflammatory Response in the Lung and Brain.

This study was performed to investigate the improving effect of a mixture of and (AASC) on cognitive dysfunction in mice with long-term exposure to fine particles (particulate matter smaller than 2.5 µm: PM). The main compounds of AASC were identified as dicaffeoylquinic acid isomers of and a quercetin-3-glucoside of .

Anti-Amnesic Effect of Synbiotic Supplementation Containing and in DSS-Induced Colitis Mice.

This study was conducted to compare the synbiotic activity between Corni fructus (C. fructus) and Limosilactobacillus reuteri (L. reuteri) on dextran sulfate sodium (DSS)-induced colitis and cognitive dysfunction in C57BL/6 mice.

Leaves of Attenuate Chronic Unpredictable Mild Stress-Induced Depression-like Behavior via Regulation of Hormonal and Inflammatory Imbalance.

This study aimed to evaluate the protective effects of ethyl acetate fraction from (EFCS) against chronic unpredictable mild stress (CUMS)-induced behavioral dysfunction and stress response in C57BL/6 mice. The physiological compounds of EFCS were identified as rutin, isoquercitrin, ethyl gallate, quercitrin, kaempferol-3-O-rhamnoside, and ethyl digallate, using UPLC-Q-TOF/MS. To evaluate the neuroprotective effect of EFCS, HO and corticosterone-induced neuronal cell viability was conducted in human neuroblastoma MC-IXC cells.

Walnut Prevents Cognitive Impairment by Regulating the Synaptic and Mitochondrial Dysfunction via JNK Signaling and Apoptosis Pathway in High-Fat Diet-Induced C57BL/6 Mice.

This study was conducted to evaluate the protective effect of (walnut, Gimcheon 1ho cultivar, GC) on high-fat diet (HFD)-induced cognitive dysfunction in C57BL/6 mice. The main physiological compounds of GC were identified as pedunculagin/casuariin isomer, strictinin, tellimagrandin I, ellagic acid-O-pentoside, and ellagic acid were identified using UPLC Q-TOF/MS analysis. To evaluate the neuro-protective effect of GC, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 2',7'-dichlorodihydrofluorecein diacetate (DCF-DA) analysis were conducted in HO and high glucose-induced neuronal PC12 cells and hippocampal HT22 cells.

Protects against PM-Induced Cognitive Dysfunction with the Regulation of Gut Function.

To evaluate the biological effects of (), we tried to confirm the possibility that the intake of could modulate cognitive and intestinal functions in PM-induced cognitive decline mice. attenuated PM-induced learning and memory impairment through antioxidant and anti-inflammatory effects by regulating the mitochondrial function and TLR-initiated NF-κB signaling. In addition, effectively alleviated Aβ production/tau phosphorylation by inhibiting the JNK phosphorylation.

Persimmon Water Extract Suppresses Hepatic Lipotoxicity by Regulating Lipid Metabolites.

This study was performed to investigate the effects of persimmon () on high-fat diet (HFD)-induced hepatic lipotoxicity. The compounds of persimmon water extract (PWE) were identified as gallic acid, glucogallin, 1-O-Galloyl-(2-O-acetyl)-glu, and trihydroxy-octadecadienoic acid. The PWE was ingested by C57BL/6 mice with an HFD for 8 weeks.

Water Extract of Protects against Fine Dust (PM)-Induced Health Damage by Regulating Gut Health.

To confirm the therapeutic effect of the water extract from (WEE) against PM induced systemic health damage, we evaluated gut health with a focus on the microbiota and metabolites. Systemic damage in mice was induced through PM exposure for 12 weeks in a whole-body chamber. After exposure for 12 weeks, body weight and food intake decreased, and WEE at 200 mg/kg body weight (mpk) alleviated these metabolic efficiency changes.

Effect of Ethyl Acetate Fraction from Leaves on PM-Induced Inflammation and Cognitive Dysfunction.

This study aimed to evaluate the protective effect of the ethyl acetate from leaves (EFEL) on PM-induced cognitive impairment in BALB/c mice. EFEL improved PM-induced cognitive decline by improving spontaneous alternative behavioral and long-term memory ability. EFEL increased ferric reducing activity power (FRAP) in serum.

Peanut (Arachis hypogaea) sprout prevents high-fat diet-induced cognitive impairment by improving mitochondrial function.

This study was performed to evaluate the improvement effect of the ethyl acetate fraction from peanut (Arachis hypogaea) sprout (EFPS) on high-fat diet (HFD)-induced cognitive deficits in C57BL/6 mice. Mice were randomly divided four groups (n = 13) as control (normal chow), HFD, EFPS 20 (20 mg/kg of body weight; intragastric administration) and EFPS 50 (50 mg/kg of body weight; intragastric administration) groups. HFD was provide for 15 weeks excepting control group.

Powdered Green Tea (Matcha) Attenuates the Cognitive Dysfunction via the Regulation of Systemic Inflammation in Chronic PM-Exposed BALB/c Mice.

This study was conducted to evaluate the anti-amnesic effect of the aqueous extract of powdered green tea (matcha) (EM) in particulate matter (PM)-induced systemic inflammation in BALB/c mice. EM ameliorated spatial learning and memory function, short-term memory function, and long-term learning and memory function in PM-induced mice. EM protected against antioxidant deficit in pulmonary, dermal, and cerebral tissues.