• Journal of Life Science
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• v.31 no.7
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• pp.677-685
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• 2021

Cannabis sativa L. belongs to the Cannabaceae family and is an annual herbaceous flowing plant. The plants can be classified into narcotic marijuana and nonnarcotic hemp. Different parts of C. sativa L. have been used as food, medicine, cosmetics, fiber and textile. However, the use of leaf, flower, and seed of C. sativa L was forbidden in Korea in January 1977 as a result of the Cannabis Control Act due to the narcotic properties. The plant's mature stems have limited uses for the production of fiber and sheets. Recently, various cannabinoids, terpenes and essential fatty acids were identified from C. sativa L., and their safety and useful bio-activities, such as neuroprotective, anti-inflammation, antithrombosis, antiepileptic, and antimicrobial activities, and the relief of pain, have been highlighted. Furthermore, the process of reduction of tetrahydrocannabinol, a representative narcotic compound, and the isolation of cannabidiol, a nonnarcotic active compound in C. sativa L., have been determined. These findings resulted in the legalization of C. sativa L. in Korea for medical use in December 2018 and the exclusion of C. sativa L. from the narcotic list of the UN Commission on Narcotics Drugs (UNCND) in December 2020. Therefore, developments of various high-value added products have commenced worldwide. Additionally, in 2021, the Korean government deregulated special zones based on hemp. In this study, the current status and the prospect of the hemp industry, as well as essential techniques for developing new hemp products, are provided for the activation of the Korea Green-Rush.

• Journal of Ginseng Research
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• v.47 no.3
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• pp.408-419
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• 2023

Background: Ginsenoside compound K (CK), the main active metabolite in Panax ginseng, has shown good safety and bioavailability in clinical trials and exerts neuroprotective effects in cerebral ischemic stroke. However, its potential role in the prevention of cerebral ischemia/reperfusion (I/R) injury remains unclear. Our study aimed to investigate the molecular mechanism of ginsenoside CK against cerebral I/R injury. Methods: We used a combination of in vitro and in vivo models, including oxygen and glucose deprivation/reperfusion induced PC12 cell model and middle cerebral artery occlusion/reperfusion induced rat model, to mimic I/R injury. Intracellular oxygen consumption and extracellular acidification rate were analyzed by Seahorse multifunctional energy metabolism system; ATP production was detected by luciferase method. The number and size of mitochondria were analyzed by transmission electron microscopy and MitoTracker probe combined with confocal laser microscopy. The potential mechanisms of ginsenoside CK on mitochondrial dynamics and bioenergy were evaluated by RNA interference, pharmacological antagonism combined with co-immunoprecipitation analysis and phenotypic analysis. Results: Ginsenoside CK pretreatment could attenuate mitochondrial translocation of DRP1, mitophagy, mitochondrial apoptosis, and neuronal bioenergy imbalance against cerebral I/R injury in both in vitro and in vivo models. Our data also confirmed that ginsenoside CK administration could reduce the binding affinity of Mul1 and Mfn2 to inhibit the ubiquitination and degradation of Mfn2, thereby elevating the protein level of Mfn2 in cerebral I/R injury. Conclusion: These data provide evidence that ginsenoside CK may be a promising therapeutic agent against cerebral I/R injury via Mul1/Mfn2 mediated mitochondrial dynamics and bioenergy.

• Korean Journal of Food Science and Technology
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• v.50 no.5
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• pp.517-527
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• 2018

The current study investigated in vitro anti-diabetic and neuroprotective effects of the ethyl acetate fraction in Actinidia arguta sprouts (EFAS), on $H_2O_2$ and high glucose-induced cytotoxicity in human neuroblastoma MC-IXC cells. EFAS had high total phenolic and total flavonoid contents. An assessment of 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging activity of EFAS, as well as its potential for inhibiting malondialdehyde production, indicated that EFAS may possess significant antioxidant properties. EFAS exerted inhibitory effects on ${\alpha}-glucosidase$ via glycemic regulation which forms advanced glycation end products. In addition, EFAS exhibited significant acetylcholinesterase inhibitory effects. Moreover, EFAS displayed protective effects against $H_2O_2$ and high glucose-induced cell death, and inhibited the generation of reactive oxygen species in MC-IXC cells. Finally, the main physiological compound of EFAS was identified via high performance liquid chromatography as a rutin.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.4
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• pp.239-246
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• 2005

In the central nervous system, nitric oxide (NO) is associated with many pathological diseases such as brain ischemia, neurodegeneration and inflammation. The epigallocatechin gallate (EGCG), a major compound of green tea, is recognized as protective substance against neuronal diseases. This study is aimed to investigate the effect of EGCG on NO-induced cell death in PC12 cells. Administration of sodium nitroprusside (SNP), a NO donor, decreased cell viability in a dose- and time-dependent manner and induced genomic DNA fragmentation with cell shrinkage and chromatin condensation. EGCG diminished the decrement of cell viability and the formation of apoptotic morphologenic changes as well as DNA fragmentation by SNP. EGCG played as an antioxidant that attenuated the production of reactive oxygen species (ROS) by SNP. The cells treated with SNP showed downregulation of Bcl-2, but upregulation of Bax. EGCG ameliorated the altered expression of Bcl-2 and Bax by SNP. The release of cytochrome c from mitochondria into cytosol and expression of voltage -dependent anion channel (VDAC)1, a cytochrome c releasing channel in mitochondria, were increased in SNP-treated cells, whereas were attenuated by EGCG. The enhancement of caspase-9, preceding mitochondria-dependent pathway, caspase-8 and death receptor-dependent pathway, as well as caspase-3 activities were suppressed by EGCG. SNP upragulated Fas and Fas-L, which are death receptor assembly, whereas EGCG ameliorated the expression of Fas enhanced by SNP. These results demonstrated that EGCG has a protective effect against SNP-induced apoptosis in PC12 cells, through scavenging ROS and regulating the mitocondria- and death receptor-mediated signal pathway. The present study suggest that EGCG might be a natural neuroprotective substance.

• Korean Journal of Food Science and Technology
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• v.46 no.4
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• pp.483-488
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• 2014

To examine the physiological effects of broccoli (Brassica oleracea var. italica) leaf, the bioavailable compounds in broccoli leaf extract, and its in vitro neuroprotective effects against $H_2O_2$-induced oxidative stress were examined in this study. The chloroform fraction of broccoli leaf extract had the highest total phenolic content of all the fraction than others, and the highest 2,2"-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical-scavenging activity and malondialdehyde (MDA) inhibitory effect. Intracellular reactive oxygen species (ROS) accumulation resulting in $H_2O_2$-treated in PC12 cells was significantly lower when the chloroform fraction was present in the medium compared to that in PC12 cells treated with $H_2O_2$ alone. In a cell viability assay performed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), the chloroform fraction showed protective effects against $H_2O_2$-induced neurotoxicity and inhibited lactate dehydrogenase (LDH) release into the medium. High-performance liquid chromatography (HPLC) analysis showed that ferulic acid was the predominant phenolic compound in chloroform fraction of broccoli leaf.

• Molecules and Cells
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• v.45 no.3
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• pp.134-147
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• 2022

The anti-oxidant enzyme heme oxygenase-1 (HO-1) is known to exert anti-inflammatory effects. From a library of pyrazolo[3,4-d]pyrimidines, we identified a novel compound KKC080096 that upregulated HO-1 at the mRNA and protein levels in microglial BV-2 cells. KKC080096 exhibited anti-inflammatory effects via suppressing nitric oxide, interleukin1β (IL-1β), and iNOS production in lipopolysaccharide (LPS)-challenged cells. It inhibited the phosphorylation of IKK and MAP kinases (p38, JNK, ERK), which trigger inflammatory signaling, and whose activities are inhibited by HO-1. Further, KKC080096 upregulated anti-inflammatory marker (Arg1, YM1, CD206, IL-10, transforming growth factor-β [TGF-β]) expression. In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinetreated mice, KKC080096 lowered microglial activation, protected the nigral dopaminergic neurons, and nigral damage-associated motor deficits. Next, we elucidated the mechanisms by which KKC080096 upregulated HO-1. KKC080096 induced the phosphorylation of AMPK and its known upstream kinases LKB1 and CaMKKbeta, and pharmacological inhibition of AMPK activity reduced the effects of KKC080096 on HO-1 expression and LPS-induced NO generation, suggesting that KKC080096-induced HO-1 upregulation involves LKB1/AMPK and CaMKKbeta/AMPK pathway activation. Further, KKC080096 caused an increase in cellular Nrf2 level, bound to Keap1 (Nrf2 inhibitor protein) with high affinity, and blocked Keap1-Nrf2 interaction. This Nrf2 activation resulted in concurrent induction of HO-1 and other Nrf2-targeted antioxidant enzymes in BV-2 and in dopaminergic CATH.a cells. These results indicate that KKC080096 is a potential therapeutic for oxidative stress-and inflammation-related neurodegenerative disorders such as Parkinson's disease.

• Korean Journal of Food Science and Technology
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• v.51 no.4
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• pp.379-392
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• 2019

The current study investigated the effect of Gabjubaekmok (Diospyros kaki) ethanolic extract (GEE) on $H_2O_2$-induced human neuroblastoma MC-IXC cells and amyloid beta $(A{\beta})_{1-42}$-induced ICR (Institute of Cancer Research) mice. GEE showed significant antioxidant activity that was evaluated based on ABTS, DPPH scavenging activity, and inhibition of malondialdehyde (MDA) and acetylcholinesterase activity. Further, GEE inhibited ROS production and increased cell viability in $H_2O_2$-induced MC-IXC cells. Administration of GEE ameliorated the cognitive dysfunction on $A{\beta}$-induced ICR mice as evaluated using Y-maze, passive avoidance, and Morris water maze tests. Results of ex vivo test using brain tissues showed that, GEE protected the cholinergic system and mitochondrial functions by increasing the levels of antioxidants such as ROS, mitochondrial membrane potential (MMP), and adenosine triphosphate (ATP) against $A{\beta}$-induced cognitive dysfunction. Moreover, GEE decreasd the expression levels of apoptosis-related proteins such as $TNF-{\alpha}$, p-JNK, p-tau, BAX and caspase 3. While, expression levels of p-Akt and $p-GSK3{\beta}$ increased than $A{\beta}$ group. Finally, gallic acid was identified as the main compound of GEE using high performance liquid chromatography.

• Food Science and Preservation
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• v.31 no.3
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• pp.452-461
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• 2024

This study evaluated the in vitro antioxidant activities of ethanolic Polygonum multiflorum (P. multiflorum) extracts and their cytoprotective effects on H₂O₂-induced HT22 and SK-N-MC cells. Among ethanolic extracts of P. multiflorum, the 40% ethanolic extract of P. multiflorum exhibited high total phenolics and flavonoid contents, with 105.68 mg of GAE/g and 28.92 mg of RE/g, respectively. The 40% ethanolic extract of P. multiflorum showed a high 2,2'-azino-bis-(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical scavenging activity and malondialdehyde (MDA) inhibitory effect. The 40% ethanolic extract of P. multiflorum also showed efficient inhibitory activity against α-glucosidase and acetylcholinesterase. Moreover, the 40% ethanolic extract of P. multiflorum reduced oxidative stress and increased cell viability in H₂O₂-induced HT22 and SK-N-MC cells as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra-zoliumbromide (MTT) and 2',7'-dichlorodihydrofluorescein diacetate (DCF-DA) assay. High-performance liquid chromatography (HPLC) identified 2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside (TSG) as the bioactive compound in the 40% ethanolic extract of P. multiflorum.