Transcriptome responses of lactic acid bacteria isolated from kimchi under hydrogen peroxide exposure.

In this study, five species of lactic acid bacteria (LAB) isolated from kimchi were analyzed in terms of their potential antioxidant activity. Latilactobacillus curvatus WiKim38, Companilactobacillus allii WiKim39, and Lactococcus lactis WiKim0124 exhibited higher radical scavenging activity, reducing power, and lipid peroxidation inhibition than the reference strain and tolerated hydrogen peroxide (H2O2) exposure up to a concentration of 2.5 mM. To investigate the antioxidant mechanism of LAB strains, transcriptomic and proteomic signatures were compared between the H2O2-exposed and untreated group using RNA sequencing and two-dimensional protein gel electrophoresis. Across all LAB strains, cell membrane responses and metabolic processes were the most prominent in the main categories of gene ontology classification, indicating that cellular components and interactions play an important role in oxidative stress responses. Thus, LAB strains isolated from kimchi could be considered for potential use in functional food production and in antioxidant starter cultures.

A Mixture of Artemisia argyi and Saururus chinensis Improves PM2.5-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 Artemisia argyi and Saururus chinensis (AASC) on cognitive dysfunction in mice with long-term exposure to fine particles (particulate matter smaller than 2.5 µm: PM2.5). The main compounds of AASC were identified as dicaffeoylquinic acid isomers of A. argyi and a quercetin-3-glucoside of S. chinesis. As a result of behavioral tests for the evaluation of cognitive function, it was confirmed that cognitive dysfunction was induced in the PM2.5 exposure group, and a tendency to improve in the AASC group was confirmed. Increased oxidative stress and inflammatory response and mitochondrial dysfunction were observed in the brain and lung tissues of the PM group. Damage to the brain and lung affected the accumulation of amyloid beta (Aß) in the brain. It increased Aß and induced the cholinergic dysfunction, hyperphosphorylation of the tau protein, and activation of apoptosis, leading to cognitive impairment. However, AASC suppressed brain and lung oxidative stress and inflammation, thereby suppressing brain Aß expression. Consequently, this study shows the potential that a steady intake of plant resources with antioxidant and anti-inflammatory activity could prevent cognitive impairment caused by PM2.5.

Anti-obesity effect of vegetable juice fermented with lactic acid bacteria isolated from kimchi in C57BL/6J mice and human mesenchymal stem cells.

This study aimed to investigate the effect of fermented vegetable juice (VJ) obtained from a blend of four crops (Brassica oleracea var. capitata, B. oleracea var. italica, Daucus carota L., and Beta vulgaris) on adipogenesis along with the identification of active compounds. Two lactic acid bacteria (LAB) (Companilactobacillus allii WiKim39 and Lactococcus lactis WiKim0124), isolated from kimchi, were used to ferment the VJ and their effectiveness was evaluated in differentiated human mesenchymal stem cells and obese mice. In vitro antibody array analysis was done to understand signaling proteins in adipogenesis. Gene Ontology enrichment analysis showed that differentially expressed proteins are related to biological processes including immunological processes. These were effectively regulated by LAB and fermented VJ. Supplementation of fermented VJ reduced the weight gain, blood biochemical indicators, and liver fat accumulation in mice. Oil Red O staining indicated that the fermentation metabolites of VJ (indole-3-lactic acid, leucic acid, and phenyllactic acid) had an inhibitory effect on lipid accumulation in vitro. Therefore, it can be concluded that LAB-fermented VJ and its metabolites have the potential to counter obesity, and thus can be therapeutically effective.

Lactic Acid Bacteria Strains Used as Starters for Kimchi Fermentation Protect the Disruption of Tight Junctions in the Caco-2 Cell Monolayer Model.

In this study, we investigated the effect of lactic acid bacteria (LAB) strains used as starters for kimchi fermentation, namely Lactococcus lactis WiKim0124, Companilactobacillus allii WiKim39, Leuconostoc mesenteroides WiKim0121 Leuconostoc mesenteroides WiKim33, and Leuconostoc mesenteroides WiKim32, on the intestinal epithelial tight junctions (TJs). These LAB strains were not cytotoxic to Caco-2 cells at 500 µg/ml concentration. In addition, hydrogen peroxide (H2O2) decreased Caco-2 viability, but the LAB strains protected the cells against H2O2-induced cytotoxicity. We also found that lipopolysaccharide (LPS) promoted Caco-2 proliferation; however, no specific changes were observed upon treatment with LAB strains and LPS. Our evaluation of the permeability in the Caco-2 monolayer model confirmed its increase by both LPS and H2O2. The LAB strains inhibited the increase in permeability by protecting TJs, which we evaluated by measuring TJ proteins such as zonula occludens-1 and occludin, and analyzing them by western blotting and immunofluorescence staining. Our findings show that LAB strains used for kimchi fermentation can suppress the increase in intestinal permeability due to LPS and H2O2 by protecting TJs. Therefore, these results suggest the possibility of enhancing the functionality of kimchi through its fermentation using functional LAB strains.

Leaves of Cedrela sinensis 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 Cedrela sinensis (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/MSE. To evaluate the neuroprotective effect of EFCS, H2O2- and corticosterone-induced neuronal cell viability was conducted in human neuroblastoma MC-IXC cells. It was found that EFCS alleviated depression-like behavior by conducting the sucrose preference test (SPT), forced swimming test (FST), open field test (OFT), and tail suspension test (TST). EFCS inhibited mitochondrial dysfunction related to neuronal energy metabolism by regulating reactive oxygen species (ROS) levels, mitochondrial membrane potential (MMP), and ATP contents in brain tissue. In addition, the administration of EFCS regulated the stress hormones in serum. EFCS regulated stress-related indicators such as CRF, ACTH, CYP11B1, and BDNF. Moreover, EFCS downregulated the inflammatory responses and apoptosis proteins such as caspase-1, TNF-α, IL-1ß, p-JNK, BAX, and p-tau in brain tissues. These results suggest that EFCS might be a potential natural plant material that alleviates CUMS-induced behavior disorder by regulating inflammation in brain tissue against CUMS-induced depression.

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 Juglans regia (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 H2O2 and high glucose-induced neuronal PC12 cells and hippocampal HT22 cells. GC presented significant cell viability and inhibition of reactive oxygen species (ROS) production. GC ameliorated behavioral and memory dysfunction through Y-maze, passive avoidance, and Morris water maze tests. In addition, GC reduced white adipose tissue (WAT), liver fat mass, and serum dyslipidemia. To assess the inhibitory effect of antioxidant system deficit, lipid peroxidation, ferric reducing antioxidant power (FRAP), and advanced glycation end products (AGEs) were conducted. Administration of GC protected the antioxidant damage against HFD-induced diabetic oxidative stress. To estimate the ameliorating effect of GC, acetylcholine (ACh) level, acetylcholinesterase (AChE) activity, and expression of AChE and choline acetyltransferase (ChAT) were conducted, and the supplements of GC suppressed the cholinergic system impairment. Furthermore, GC restored mitochondrial dysfunction by regulating the mitochondrial ROS production and mitochondrial membrane potential (MMP) levels in cerebral tissues. Finally, GC ameliorated cerebral damage by synergically regulating the protein expression of the JNK signaling and apoptosis pathway. These findings suggest that GC could provide a potential functional food source to improve diabetic cognitive deficits and neuronal impairments.

Korean Red Pine (Pinus densiflora) Bark Extract Attenuates Aß-Induced Cognitive Impairment by Regulating Cholinergic Dysfunction and Neuroinflammation.

In this study, we investigated the anti-amnesic effect of Korean red pine (Pinus densiflora) bark extract (KRPBE) against amyloid beta1-42 (Aß1-42)-induced neurotoxicity. We found that treatment with KRPBE improved the behavioral function in Aß-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 Aß and phosphorylated tau (p-tau) and inflammatory cytokines TNF-α, p-IκB-α, and IL-1ß. 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 Aß1-42-induced cognitive impairment in mice.

Porphyra tenera Protects against PM2.5-Induced Cognitive Dysfunction with the Regulation of Gut Function.

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 Aß 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.

Water Extract of Ecklonia cava Protects against Fine Dust (PM2.5)-Induced Health Damage by Regulating Gut Health.

To confirm the therapeutic effect of the water extract from Ecklonia cava (WEE) against PM2.5 induced systemic health damage, we evaluated gut health with a focus on the microbiota and metabolites. Systemic damage in mice was induced through PM2.5 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, PM2.5 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 PM2.5 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 PM2.5 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 PM2.5 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 PM2.5 induced health damage by regulating gut function.

Persimmon Water Extract Suppresses Hepatic Lipotoxicity by Regulating Lipid Metabolites.

This study was performed to investigate the effects of persimmon (Diospyros kaki) 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. The PWE improved glucose tolerance and suppressed weight gain by inhibiting increases in the weight of liver and adipose tissues. The results of serum biomarker analysis showed that PWE suppressed biomarkers such as liver injury and dyslipidemia. In ex vivo tests, reduction of oxidative stress and improvement of mitochondrial dysfunction were confirmed in the liver of PWE groups. In a molecular study, it was confirmed that PWE decreased lipid accumulation, insulin resistance, inflammation, and apoptosis in the liver. Finally, in a metabolite analysis of liver tissue using ultra-high performance liquid chromatography with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS), it was confirmed that PWE has an effect on lipid metabolism. In particular, PWE reduced phosphatidylcholines (PCs) and lysophosphatidylcholines (lysoPCs). Notably, it is presumed that the reduction of lysoPCs and PCs in the PWE group is related to the improvement of liver dysfunction due to lipotoxicity.

Effect of Ethyl Acetate Fraction from Eucommia ulmoides Leaves on PM2.5-Induced Inflammation and Cognitive Dysfunction.

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.

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. 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.

Powdered Green Tea (Matcha) Attenuates the Cognitive Dysfunction via the Regulation of Systemic Inflammation in Chronic PM2.5-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)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.

Mixture of Phlorotannin and Fucoidan from Ecklonia cava Prevents the Aß-Induced Cognitive Decline with Mitochondrial and Cholinergic Activation.

The anti-amnesic effect of a mixture (4:6 = phlorotannin:fucoidan from Ecklonia cava, P4F6) was evaluated on amyloid-beta peptide (Aß)-induced cognitive deficit mice. The cognitive function was examined by Y-maze, passive avoidance, and Morris water maze tests, and the intake of the mixture (P4F6) showed an ameliorating effect on Aß-induced learning and memory impairment. After the behavioral tests, superoxide dismutase (SOD) activity and thiobarbituric acid-reactive substances (TBARS) contents were confirmed in brain tissue, and in the results, the mixture (P4F6) attenuated Aß-induced oxidative stress. In addition, mitochondrial activity was evaluated by mitochondrial reactive oxygen species (ROS) content, mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic signaling pathway, and the mixture (P4F6) enhanced mitochondrial function. Furthermore, the mixture (P4F6) effectively regulated tau hyperphosphorylation by regulating the protein kinase B (Akt) pathway, and promoted brain-derived neurotrophic factor (BDNF) in brain tissue. Moreover, in the cholinergic system, the mixture (P4F6) ameliorated acetylcholine (ACh) content by regulating acetylcholinesterase (AChE) activity and choline acetyltransferase (ChAT) expression in brain tissue. Based on these results, we suggest that this mixture of phlorotannin and fucoidan (P4F6) might be a substance for improving cognitive function by effectively regulating cognition-related molecules.

Immature Persimmon Suppresses Amyloid Beta (Aß) Mediated Cognitive Dysfunction via Tau Pathology in ICR Mice.

This study confirmed the ameliorating effect of immature persimmon (Diospyros kaki) ethanolic extract (IPEE) on neuronal cytotoxicity in amyloid beta (Aß)1-42-induced ICR mice. The administration of IPEE ameliorated the cognitive dysfunction in Aß1-42-induced mice by improving the spatial working memory, the short-term and long-term memory functions. IPEE protected the cerebral cholinergic system, such as the acetylcholine (ACh) level and acetylcholinesterase (AChE) activity, and antioxidant system, such as the superoxide dismutase (SOD), reduced glutathione (GSH) and malondialdehyde (MDA) contents. In addition, mitochondrial dysfunction against Aß1-42-induced toxicity was reduced by regulating the reactive oxygen species (ROS), mitochondrial membrane potential and ATP contents. In addition, IPEE regulated the expression levels of tau signaling, such as TNF-α, p-JNK, p-Akt, p-GSK3ß, p-tau, p-NF-κB, BAX and caspase 3. Finally, gallic acid, ellagic acid and quercetin 3-O-(6″-acetyl-glucoside) were identified as the physiological compounds of IPEE using ultra-performance liquid chromatography ion mobility separation quadrupole time-of-flight/tandem mass spectrometry (UPLC IMS Q-TOF/MS2).

Ecklonia cava Attenuates PM2.5-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect.

To evaluate the effects of Ecklonia cava (E. cava) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM2.5). The intake of water extract from E. cava (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM2.5 exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM2.5-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM2.5-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2'-phloroeckol.

Ameliorative effect of persimmon (Diospyros kaki) in cognitively impaired diabetic mice.

The effects of ethanolic extract of Diospyros kaki (EED) on diabetic cognitive impairment were investigated in high-fat diet (HFD)-induced mouse. After HFD was fed to mouse for 16 weeks, EED was administrated to mouse for 4 weeks. EED reduced fasting blood glucose level and improved cognitive and behavioral dysfunction. EED improved serum biomarkers related to lipid and liver damage better than positive control (PC). In addition, EED ameliorated impaired cholinergic system, increased oxidative stress as well as mitochondrial dysfunction compared with HFD group. In the molecular study, EED downregulated the phosphorylation of c-Jun N-terminal kinase (p-JNK), which phosphorylates the serine residue of insulin receptor substrate-1 (IRS-1pSer). Finally, various physiological compounds such as tannin-based ingredients were identified using UPLC-QTOF/MS2 . These results suggest that EED can help improve cognitive impairment caused by HFD. PRACTICAL APPLICATIONS: Recently, cognitive impairment caused by type 2 diabetes mellitus (T2DM) has become a problem. T2DM, mainly derived from HFD, is characterized by hyperglycemia, which is associated with insulin resistance. In this study, EED not only improved hyperglycemia and insulin resistance, but also restored diabetes-related cognitive dysfunction in HFD-induced diabetic mice. Finally, the decrease in cholinergic and antioxidant systems related to cognitive impairment was recovered by consumption of EED via improvement of insulin signaling pathway. Therefore, this study suggests that persimmon (Diospyros kaki) containing diverse physiological compounds has potential and industrial value as a functional food material for cognitive improvement.

Can unrecognized fecal loading without infrequent bowel movements be a cause of symptoms in a subset of patients with functional bowel disorders?

Infrequent bowel movements are a common feature of constipation, but fecal loading as a cause of symptoms in patients with regular bowel movements has not previously been evaluated. The aim of this preliminary study was to assess prospectively if fecal loading may be a cause of bowel symptoms in patients with regular bowel movements. Consecutive patients attending a gastroenterology clinic for functional bowel symptoms (FBD) not including infrequent bowel movements and who did not fulfil the criteria for constipation-predominant irritable bowel syndrome or functional constipation underwent plain abdominal radiography. Those with fecal loading received dietary advice and laxative treatment. The reproducibility of determination of fecal loading using the Leech score was assessed 'blindly' by a consultant radiologist. Twenty-six of 74 patients with FBD but not infrequent bowel movements had fecal loading demonstrated on abdominal radiology. Their Leech scores were significantly higher than those of control patients matched for age, sex and hospital (median 6 vs. 4, IQR 5-7 vs. 3.5-5, p < 0.001). Three out of 20 patients (15%) who returned for review after dietary advice and laxatives were asymptomatic and 17/20 (85%) had improved. Fecal loading may therefore cause bowel symptoms in patients who move their bowels regularly and dietary and laxative treatment may then improve these symptoms. This approach may prove cost-effective as an empirical interim measure especially where healthcare resources are limited and where sophisticated imaging is not readily available.

Actinidia arguta Sprout as a Natural Antioxidant: Ameliorating Effect on Lipopolysaccharide-Induced Cognitive Impairment.

Here, we investigated the prebiotic and antioxidant effects of Actinidia arguta sprout water extract (AASWE) on lipopolysaccharide (LPS)-induced cognitive deficit mice. AASWE increased viable cell count, titratable acidity, and acetic acid production in Lactobacillus reuteri strain and showed a cytoprotective effect on LPS-induced inflammation in HT-29 cells. We assessed the behavior of LPSinduced cognitive deficit mice using Y-maze, passive avoidance and Morris water maze tests and found that administration of AASWE significantly improved learning and memory function. The AASWE group showed antioxidant activity through downregulation of malondialdehyde levels and upregulation of superoxide dismutase levels in brain tissue. In addition, the AASWE group exhibited activation of the cholinergic system with decreased acetylcholinesterase activity in brain tissue. Furthermore, AASWE effectively downregulated inflammatory mediators such as phosphorylated- JNK, phosphorylated-NF-κB, TNF-α and interleukin-6. The major bioactive compounds of AASWE were identified as quercetin-3-O-arabinopyranosyl(1→2)-rhamnopyranosyl(1→6)-glucopyranose, quercetin-3-O-apiosyl(1→2)-galactoside, rutin, and 3-caffeoylquinic acid. Based on these results, we suggest that AASWE not only increases the growth of beneficial bacteria in the intestines, but also shows an ameliorating effect on LPS-induced cognitive impairment.

Matcha Improves Metabolic Imbalance-Induced Cognitive Dysfunction.

This study was conducted to assess the protective effect of extract of match (EM) on high-fat diet- (HFD-) induced cognitive deficits in male C57BL/6 mice. It was found that EM improved glucose tolerance status by measuring OGTT and IPGTT with HFD-induced mice. EM protected behavioral and memory dysfunction in Y-maze, passive avoidance, and Morris water maze tests. Consumption of EM reduced fat mass, dyslipidemia, and inflammation in adipose tissue. Also, EM ameliorated hepatic and cerebral antioxidant systems. EM improved the cerebral cholinergic system by regulating ACh contents and expression of AChE and ChAT. Also, EM restored mitochondrial function in liver and brain tissue. EM attenuated hepatic inflammatory effect, lipid synthesis, and cholesterol metabolism by regulating the protein expression of TNF-α, TNFR1, p-IRS-1, p-JNK, IL-1ß, iNOS, COX-2, HMGCR, PPARγ, and FAS. Finally, EM regulated cognitive function and neuroinflammation in the whole brain, hippocampus, and cerebral cortex by regulating the protein expression of p-JNK, p-Akt, p-tau, Aß, BDNF, IDE, COX-2, and IL-1ß. These findings suggest that EM might be a potential source of functional food to improve metabolic disorder-associated cognitive dysfunction.