• Journal of Oriental Neuropsychiatry
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• v.22 no.4
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• pp.201-218
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• 2011

Objectives : The aim of this study was to investigate the effects of Guibi-Tang(GBT) on focal brain ischemic injury induced by intraluminal filament insertion in rats. Methods : The ischemia was induced by intraluminal filament insertion into middle cerebral artery. Sprague-Dawley rats were divided into five groups, normal group(n=8); control group was ischemia induced and no treatment(n=8); GBT 1X group was ischemia induced and administrated 42.2 mg/ml/kg of Guibi-Tang orally(n=8); GBT 3X group was ischemia induced and administrated 126.6 mg/ml/kg of Guibi-Tang orally(n=8); GBT 6X group was ischemia induced and administrated 253.2 mg/ml/kg of Guibi-Tang orally(n=8) for 21 days. mGluR5, Bax, Bcl-2 and cytochrome C were investigated to observe the effects of Guibi-Tang on apoptosis. The effects of Guibi-Tang on neuroprotective/apoptotic agents in cresyl violet, choline acetyltranferase(ChAT) with ischemic injury were investigated. Results : The intensity of mGluR5 mRNA in the hippocampal CA1 was increased in normal and GBT(Guibi-Tang) 1X groups compared with the control group. The intensity of Bax mRNA in the hippocampal CA1 was decreased in normal and GBT 1X groups compared with the control group. However it was increased unexpectedly in GBT 3X group. The intensity of Bcl-2 mRNA in the hippocampal CA1 was increased in normal and GBT 1X groups compared with the control group. The intensity of Bax/Bcl-2 ratio in the hippocampal CA1 was decreased in normal and GBT 1X groups compared with the control group. The intensity of cytochrome C protein in the hippocampal CA1 was decreased in normal, GBT 1X and GBT 6X groups compared with the control group. The density of neurons stained by cresyl violet and ChAT was increased in normal and GBT 1X groups compared with the control group. Conclusions : These results suggest that Guibi-Tang may have protective effect on vascular dementia.

• Journal of Life Science
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• v.29 no.11
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• pp.1200-1207
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• 2019

Ultraviolet radiation exposure is a major cause of extrinsic skin aging, which leads to skin hyperpigmentation. Loganin, a major iridoid glycoside obtained from Corni fructus, has anti-inflammatory, anti-diabetic, and neuroprotective effects. In this study, we investigated the mechanisms underlying the anti-melanogenic effects of loganin in B16F10 melanocytes treated with ${\alpha}$-melanocyte stimulating hormone (${\alpha}-MSH$) and 3-isobutyl-1-methylxanthine (IBMX). Anti-melanogenic activity was measured by treating cells with loganin at concentrations between 1 and $20{\mu}m$. Cell viability assays confirmed that doses of loganin up to $20{\mu}m$ were not cytotoxic. Loganin significantly and dose-dependently decreased intracellular melanin production. We also investigated potential molecular signaling pathways for the anti-melanogenesis effects of loganin. Western blotting showed that treatment with ${\alpha}-MSH$ and IBMX increased the phosphorylation of cAMP response element-binding protein (CREB) and the gene expressions of microphthalmia-associated transcription factor (MITF) and tyrosinase. Addition of loganin suppressed these increases, while promoting the phosphorylation of extracellular signal regulated kinase (ERK) and the anti-melanogenesis response. Our data therefore indicated that loganin could attenuate the increased melanin synthesis induced by ${\alpha}-MSH$ and IBMX treatment of B16F10 melanocytes. This attenuation appears to occur by downregulation of CREB phosphorylation and MITF and tyrosinase gene expression and upregulation of ERK phosphorylation. These finding suggests that loganin could be a valuable candidate for treatment of skin diseases related to hyperpigmentation.

• Korean Journal of Plant Resources
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• v.23 no.2
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• pp.165-171
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• 2010

Oxidative stress induced by reactive oxygen intermediates has been implicated in a variety of human diseases including neurodegenerative disorders, cancer, cardiovascular and respiratory diseases, and mode of action of environmental toxicants. Tert-butylhydroperoxide (t-BHP) is an organic lipid hydroperoxide analogue, which is commonly used as a pro-oxidant for evaluating mechanisms involving oxidative stress in cells and tissues. In this study, the underlying mechanisms involved in the protective effects of Hwabuk 94 kiwifruit (Actinidia deliciosa cv. 'Hwabuk 94'), which is cultivated in Jeju, on the t-BHP-induced cytotoxicity in PC12 cell. The pretreatment of rat pheochromocytoma cell line PC12 with Hwabuk 94 extract ($1-100\;{\mu}g/ml$) resulted in a significant recovery from t-BHP-induced cell death and increased Bcl-2 and procaspase-3 expression, whereas the expression of Bax and cleaved PARP were decreased in a dose-dependent manner compared to the control. Furthermore, Hwabuk 94 inhibited the t-BHP-induced p38 MAP kinase and extracellular signal-regulated kinase 1/2, but not c-Jun N-terminal kinase activations. Finally, these findings suggest that Hwabuk 94 kiwifruit might attenuate t-BHP-induced PC12 cell cytotoxicity, at least in part, through the inhibition of signaling pathways mediated by the ERK1/2 and p38 MAP kinase.

• Journal of Microbiology and Biotechnology
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• v.32 no.7
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• pp.927-937
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• 2022

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.

• Journal of the Korean Applied Science and Technology
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• v.38 no.6
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• pp.1543-1552
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• 2021

Atractylodes japonica has been widely used in a traditional Korean herbal medicine exerting various pharmacological activities such as diauretic action, asriction, anti-allergy, neuroprotective activity, anti-cancer, immunomodulation and gastrointestinal protective effect. This study was to investigate the antioxidant, nitric oxide and inflammatory cytokines production of A. japonica extract by water and 70% ethanol. DPPH and ABTS free radical scavenging activity were increased in a dose-dependent manners with both extracts and there was no difference with extract solvents. 70% ethanol extract of A. japonica showed a very strong inhibitory effect on NO production. Both extracts of A. japonica significantly reduce the expression of iNOS and COX-2 proteins involved in NO prodction. A. japonica extract by water and 70% ethanol inhibited LPS-induced proinflammatory cytokines such as IL-6 and IL-1b. In this study, 70% ethanol extract of A. japonica significantly suppresses LPS-induced NO and inflammatory cytokine production. Therefore it can be widely used to treat and improve inflammatory diseases.

• Korean Journal of Food Science and Technology
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• v.50 no.4
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• pp.383-390
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• 2018

Most neurodegenerative diseases are known to be influenced by oxidative stress. We investigated the anti-oxidative activity of the concentrate of fermented wild ginseng root culture (HLJG0701) containing ginsenosides Rg5 and Rk1. HLJG0701 showed effective DPPH and ABTS radical scavenging ability ($IC_{50}$: 16- and 4-fold dilution, respectively) and was inhibited dose-dependently by the $FeSO_4$-induced lipid peroxidation group (8- and 4-fold dilution: 2.3 and 1.5 nM, respectively). In MTT and LDH assays, 8-, 16-, 32- and 64-fold diluted HLJG0701 significantly increased cell viability by 70, 53, 35, and 26%, respectively. LDH released by HLJG0701 was reduced 1.3-fold with 8-fold diluted HLJG0701 compared to the $H_2O_2$-treated control. In addition, the inhibitory effect of HLJG0701 on oxidative stress in PC12 cells was confirmed by DCF-DA analysis (16-, 4-fold diluted HLJG0701: 50 and 68% ROS inhibition, respectively), TBARS (16- and 4-fold diluted HLJG0701: 50.7 and 46.5% inhibition, respectively), GPx (16- and 4-fold diluted HLJG0701: 133.3 and 227.3% release, respectively), and SOD analysis (16- and 4-fold diluted HLJG0701: 118.2 and 218.2% release, respectively). These results suggested that HLJG0701 protects neuronal cells by its anti-oxidative effects and hence can be a potential preventive material against neurodegenerative diseases.

• Korean Journal of Food Science and Technology
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• v.42 no.4
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• pp.481-487
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• 2010

The nutritional components, antioxidant, and neuroprotective effects of water and a 50% methanol extract from litchi fruit pericarp were investigated. The most abundant mineral, amino acid, and fatty acid were K, proline, and palmitic acid, respectively. In addition, the total water phenolics and 50% methanol extracts were 8.02 and 12.28 mg/g, respectively. The DPPH, ABTS radical scavenging activities and ferric reducing antioxidant power of the water and 50% methanol extracts showed dose-dependent antioxidant activity. In a cell viability assay using MTT, almost all extracts showed a protective effect against $H_2O_2$-induced neurotoxicity, and lactate dehydrogenase leakage was also inhibited by the pericarp extracts. In particular, the 50% methanol extract showed a higher cell membrane protective effect than the water extract at the highest concentration. Consequently, these data suggest that litchi fruit pericarp can be utilized as an effective and safe functional food substances for natural antioxidants and may reduce the risk of neurodegenerative disorders.

• Journal of the korean academy of Pediatric Dentistry
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• v.33 no.1
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• pp.13-24
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• 2006

Neuronal apoptotic events, consequently resulting in neuronal cell death, are occurred in hypoxic/ischemic condition. This cell death has been shown to be accompanied with the production of reactive oxygen species (ROS), which can attack cellular components such as nucleic acids, proteins and phospholipid. However, the underlying mechanisms of apoptosis induced in hypoxic/ischemic condition and its treatment methods are unsettled. Cobalt chloride $(CoCl_2)$ has been known to mimic hypoxic condition including the production of ROS. Epigallocatechin gallate (EGCG), a green tea polyphenol, has diverse pharmacologial activities in cell growth and death. This study was aimed to investigate the apoptotic mechanism by $CoCL_2$ and effects of EGCG on $CoCl_2-induced$ apoptosis in PC12 cells. Administration of $CoCl_2$ decreased cell survival in dose- and time-dependent manners and induced genomic DNA fragmentation. Treatment with $100{\mu}M$ EGCG for 30 min before PC12 cells were exposed to $150{\mu}M$ $CoCl_2$, being resulted in the cell viability and DNA fragmentation being rescued. $CoCl_2$ caused morphologic changes such as cell swelling and condensed nuclei whereas EGCG attenuated morphologic changes by $CoCl_2$. EGCG suppressed the apoptotic peak and a loss of ${\Delta}{\psi}_m$ induced by $CoCl_2$. $CoCl_2$ decreased Bcl-2 expression but Bax expression was not changed in $CoCl_2$- treated cells. EGCG attenuated the Bcl-2 underexpression by $CoCl_2$. $CoCl_2$ augumented the cytochrome c release from mitochondria into cytoplasm and increased caspase-8, -9 and caspase-3 activity a marker of the apoptotic executing stage. EGCG ameliorated the incruement in caspase-8, -9 and -3 activity, and cytochrome c release by $CoCl_2$ NAC (N-acetyl-cysteine), a scavenger of ROS, attenuated $CoCl_2-induced$ apoptosis in consistent with those of EGCG. These results suggest that $CoCl_2$ induces apoptotic cell death through both mitochondria- and death receptor-dependent pathway and EGCG has neuroprotective effects against $CoCl_2-induced$ apoptosis in PC12 cells.

• Korean Journal of Food Science and Technology
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• v.44 no.4
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• pp.428-433
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• 2012

Probiotics and their products, such as yogurt and cheese have been widely consumed in many countries with proven health benefits including anti-microbial activity and anti-diarrheal activity. LHFM (Lactobacillus helveticus - fermented milk) is a processed skim milk powder, fermented by a probiotics, L. helveticus IDCC3801. In the present study, we aimed to investigate the neuroprotective effects and the cognitive improvements of LHFM. LHFM itself did not show any cytotoxicity to the human neuroblastoma cell line, SH-SY5Y; however, it dose-dependently protected against glutamate-induced neuronal cell death. LHFM also attenuated scopolamine-induced memory deficit in Y-maze and Morris-water maze. In the analysis of hippocampus after a behavior test, LHFM significantly increased the acetylcholine level and also inhibited acetylcholine esterase activity. Therefore, the raised acetylcholine release partially contributes to the improvement of learning and memory by a treatment with LHFM. These results suggest that LHFM is an effective material for prevention or improvement of cognitive impairments caused by neuronal cell damage and central cholinergic dysfunction.

• Journal of Life Science
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• v.31 no.11
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• pp.987-994
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• 2021

Our previous studies have reported that antimicrobial peptides (AMPs) derived from the larvae of white-spotted flower chafer (Protaetia brevitarsis seulensis) exert anti-inflammatory and neuroprotective activities. This study explored the anti-inflammatory effects of protaetiamycine 9 (CVLKKAYFLTNLKLRG-NH₂), a novel AMP, derived from P. b. seulensis against lipopolysaccharide (LPS)-mediated inflammatory response in RAW264.7 macrophage cells. Protaetiamycine 9 (25, 50, 75, and 100 ㎍/ml) did not cause cytotoxic effects against RAW264.7 cells. The RAW264.7 cells were pre-treated with various concentrations of protaetiamycine 9 (25-100 ㎍/ml) for 1 hr and then exposed to LPS (100 ng/ml) for 24 hr. Protaetiamycine 9 treatments decreased the LPS-induced secretion of inflammatory mediators, such as nitric oxide (NO), in a dose-dependent manner. Protaetiamycine 9 (25-100 ㎍/ml) effectively downregulated the LPS-induced increase in mRNA and the protein expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), which are involved in the production of inflammatory mediators. Protaetiamycine 9 also suppressed the production and gene expression of pro-inflammatory cytokines, including interleukin (IL)-6 and IL-1β, compared to the presence of LPS alone. Furthermore, protaetiamycine 9 inhibited the degradation of inhibitory kappa B alpha (IκB-α) and the phosphorylation of mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. In conclusion, these results suggest that protaetiamycine 9 exhibits LPS-mediated inflammatory responses by blocking IκB-α degradation and MAPK phosphorylation.