This study was conducted to evaluate the anti-amnesic effect of the aqueous extract of powdered green tea (matcha) (EM) in particulate matter (PM)2.5-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 PM2.5-induced mice. EM protected against antioxidant deficit in pulmonary, dermal, and cerebral tissues. In addition, EM improved the cholinergic system through the regulation of acetylcholine (ACh) levels and acetylcholinesterase (AChE) activity in brain tissue, and it protected mitochondrial dysfunction by regulating the production of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and ATP contents in brain tissue. EM attenuated systemic inflammation and apoptotic signaling in pulmonary, dermal, olfactory bulb, and hippocampal tissues. Moreover, EM suppressed neuronal cytotoxicity and cholinergic dysfunction in hippocampal tissue. This study suggests that EM might be a potential substance to improve PM2.5-induced cognitive dysfunction via the regulation of systemic inflammation.

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. C. fructus (as prebiotics, PRE), L. reuteri (as probiotics, PRO), and synbiotics (as a mixture of L. reuteri and C. fructus, SYN) were fed to mice for 3 weeks. Consumption of PRE, PRO, and SYN ameliorated colitis symptoms in body weight, large intestinal length, and serum albumin level. Moreover, SYN showed a synergistic effect on intestinal permeability and intestinal anti-inflammation response. Also, SYN significantly improved cognitive function as a result of measuring the Y-maze and passive avoidance tests in DSS-induced behavioral disorder mice. Especially, SYN also restored memory function by increasing the cholinergic system and reducing tau and amyloid β pathology. In addition, PRE, PRO, and SYN ameliorated dysbiosis by regulating the gut microbiota and the concentration of short-chain fatty acids (SCFAs) in feces. The bioactive compounds of C. fructus were identified with quinic acid, morroniside, loganin, and cornuside, using ultra-performance liquid chromatography-quadrupole time-of-flight tandem mass spectrometry (UPLC-Q-TOF-MS2). In conclusion, synbiotic supplementation alleviated DSS-induced colitis and cognitive dysfunction by modulating gut microbiota, proinflammatory cytokines, and SCFAs production.

This study aimed to evaluate the protective effect of the ethyl acetate from Eucommia ulmoides leaves (EFEL) on PM2.5-induced cognitive impairment in BALB/c mice. EFEL improved PM2.5-induced cognitive decline by improving spontaneous alternative behavioral and long-term memory ability. EFEL increased ferric reducing activity power (FRAP) in serum. In addition, EFEL increased superoxide dismutase (SOD) and reduced glutathione (GSH) contents and inhibited the production of malondialdehyde (MDA) in lung and brain tissues. EFEL also restored the mitochondrial function by regulating reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) level, and ATP level in lung and brain tissues. EFEL ameliorated the cholinergic system by regulating the acetylcholine (ACh) content and acetylcholinesterase (AChE) activity in the brain tissue and the expression of AChE and choline acetyltransferase (ChAT) in the whole brain and hippocampal tissues. EFEL reduced PM2.5-induced excessive expression of inflammatory protein related to the lung, whole brain, olfactory bulb, and hippocampus. Physiological compounds of EFEL were identified as 5-O-caffeolyquinic acid, rutin, quercetin, and quercetin glycosides. As a result, EFEL has anti-inflammation and anti-amnesic effect on PM2.5-induced cognitive impairment by regulating the inflammation and inhibiting the lung and brain tissue dysfunction, and its effect is considered to be due to the physiological compounds of EFEL.

This study aimed to evaluate the antioxidant and hepatoprotective effects of aqueous and 60% ethanol extracts of Allium ochotense Prokh. against alcohol-induced cytotoxicity as well as on the activities of alcohol-metabolic enzymes. Antioxidant effects of the extracts were analyzed using 3-ethylbenzothiazoline-6-sulfonic acid, 1,1-diphenyl-2-picrylhydrazl, ferric reducing antioxidant power, and malondialdehyde assays, and found that both extracts exhibited considerable antioxidant activities. Additionally, both extracts showed synergistic effects on the activities of alcohol-metabolic enzymes, such as alcohol dehydrogenase, but not on the activity of aldehyde dehydrogenase. In addition, 2’-7’-dichlorodihydrofluorescein diacetate (DCF-DA) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays revealed that aqueous and 60% ethanol extracts reduced oxidative stress and increased cell viability. Moreover, both extracts regulated the expression of apoptosis-related proteins, namely B-cell lymphoma (BCl-2), BCl-2 associated X (BAX), and pro-caspase-3, in HepG2 cells. In conclusion, aqueous and 60% ethanol extracts of A. ochotense Prokh. might be valuable functional materials derived from natural resources for the prevention of ethanol-induced cytotoxicity.

To evaluate the biological effects of Porphyra tenera (P. tenera), we tried to confirm the possibility that the intake of P. tenera could modulate cognitive and intestinal functions in PM2.5-induced cognitive decline mice. P. tenera attenuated PM2.5-induced learning and memory impairment through antioxidant and anti-inflammatory effects by regulating the mitochondrial function and TLR-initiated NF-κB signaling. In addition, P. tenera effectively alleviated Aβ production/tau phosphorylation by inhibiting the JNK phosphorylation. Also, the bioactive constituents of P. tenera determined the sulfated galactan, mycosporine-like amino acids (MAAs), and chlorophyll derivatives. Moreover, the bioactive compounds of P. tenera by gut fermentation protected against gut dysbiosis and intestinal tight junction damage with a decrease in inflammatory response and short-chain fatty acid production. Based on these results, our findings suggest that P. tenera with sulfated galactan and MAAs is a potential material for cognitive function improvement.

To confirm the therapeutic effect of the water extract from Ecklonia cava (WEE) against PM 2.5 induced systemic health damage, we evaluated gut health with a focus on the microbiota and metabolites. Systemic damage in mice was induced through PM 2.5 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. In addition, PM 2.5 induced changes in the length of the colon and fecal water content. The administration of the WEE at 200 mpk oral dose effectively reduced changes in the colon caused by PM 2.5 exposure. We also attempted to confirm whether the effect of the WEE is mediated via regulation of the microbiota-gut-brain axis in mice with PM 2.5 induced systemic damage. We examined changes in the fecal microbiota and gut metabolites such as short-chain fatty acids (SCFAs) and kynurenine metabolites. In the PM 2.5 exposed group, a decrease in the abundance of Lactobacillus (Family: Lactobacillaceae) and an increase in the abundance of Alistipes (Family: Rikenellaceae) were observed, and the administration of the WEE showed a beneficial effect on the gut microbiota. In addition, the WEE effectively increased the levels of SCFAs (acetate, propionate, and butyrate). Furthermore, kynurenic acid (KYNA), which is a critical neuroprotective metabolite in the gut-brain axis, was increased by the administration of the WEE. Our findings suggest that the WEE could be used as a potential therapeutic against PM 2.5 induced health damage by regulating gut 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. EFPS ameliorated cognitive dysfunction in Y-maze, passive avoidance test and Morris water maze test. EFPS significantly improved glucose tolerance and serum lipid profile, and reduced body weight. EFPS ameliorated oxidative stress by regulating MDA levels and SOD activity in liver and brain tissues. In addition, EFPS restored brain mitochondrial dysfunction related to energy metabolism. Moreover, the bioactive compounds of EFPS were identified as di-caffeic acid, caffeic acid, dihydrokaempferol-hexoside, di-p-coumaroyl tartaric acid isomer and group B soyasaponins using ultra-performance liquid chromatography-quadrupole-time-of-flight (UPLC-Q-TOF) mass spectrometry. These results show that EFPS can improve cognitive functions in HFD-induced diabetic mice.

This study aimed to assess the protective effect of an extract of Lonicera japonica against particulate-matter (PM)2.5-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/MSE). The extract of Lonicera japonica reduced cell death, reactive oxygen species (ROS) production, and inflammation in A549 cells. The extract of Lonicera japonica decreased serum T cells, including CD4+ T cells, CD8+ T cells, and total T helper 2 (Th2) cells, and immunoglobulins, including immunoglobulin G (IgG) and immunoglobulin E (IgE), in PM2.5-induced BALB/c mice. The extract of Lonicera japonica protected the pulmonary antioxidant system by regulating superoxide dismutase (SOD) activity, reduced glutathione (GSH) contents, and malondialdehyde (MDA) levels. In addition, it ameliorated mitochondrial function by regulating the production of ROS, mitochondrial membrane potential (MMP), and ATP contents. Moreover, the extract of Lonicera japonica exhibited a protective activity of apoptosis, fibrosis, and matrix metalloproteinases (MMPs) via TGF-β and NF-κB signaling pathways in lung tissues. This study suggests that the extract of Lonicera japonica might be a potential material to improve PM2.5-induced pulmonary inflammation, apoptosis, and fibrosis.