• Therapeutic Science for Rehabilitation
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• v.11 no.4
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• pp.41-53
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• 2022

Objective : The purpose of this study is to identify and analyze the vocational rehabilitation evaluation tool for the mentally disabled. Methods : For literature search, the Pubmed database was used, and for the analysis, the development year, evaluation method, number of items, scale, and evaluation items were analyzed. In the analysis method, each evaluation item was divided into four categories: function, internal factor, environment, and mental symptom, and the evaluation elements of each evaluation tool were identified. Results : When searching Pubmed through search terms, 161 documents were retrieved. According to the selection method, Griffiths Work Behavior Scale (GWBS), Occupational Functioning Scale (OFS), Social and Occupational Functioning Assessment Scale (SOFAS), Work Ability Index (WAI), Work Behavior Inventory (WBI), Work Environment Impact Scale (WEIS), and Work and Social Adjustment Scale (WSAS) were screened. The evaluation items of all evaluation tools included job-related functional evaluation. According to the purpose of each evaluation tool, internal factors, environment, and mental symptoms were measured. Conclusion : Occupational skills are skills in which various functions such as physical, cognitive, social skills, and coping skills act in a complex way. Therefore, it is necessary to include the four factors analyzed in this study: function, internal factors, environment, and psychiatric symptoms.

• The Korea Journal of Herbology
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• v.38 no.1
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• pp.11-19
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• 2023

Objectives : Neuroinflammation is a common pathological mechanism of neurodegenerative diseases, and the development of therapeutic agents is urgently needed. Red ginseng has been known to be good for the immune stimulation in Eastern Asia. Although the immuno-stimulatory activity of red ginseng are already known, the neuro-protective effects of cultivated red ginseng with fermented complex mushroom-cereal mycelium (RGFM) have not been conducted. Thus, in this study, we tried to investigate the anti-neuroinflammatory effect of RGFM water extract on lipopolysaccharide (LPS) stimulated BV2 cells. Methods : BV2 cells were pretreated with RGFM 1 h prior to LPS exposure. To determine the neuro-protective effects of RGFM water extract, we measured the expression of inflammatory mediators including inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and nitric oxide (NO) and pro-inflammatory cytokines such as interleukin (IL)-1𝛽, IL-6 and tumor necrosis factor (TNF)-𝛼 in LPS-stimulated BV2 cells. In addition, to find out the regulatory mechanism of RGFM water extract, we assessed the protein levels of mitogen-activated protein kinases (MAPKs) and inhibitory 𝜅B𝛼 (I𝜅B𝛼) by western blotting. Results : In our study, treatment of RGFM reduced the mRNA expression of iNOS and COX-2 and suppressed NO production in LPS-stimulated BV2 cells. Additionally, the secretion of IL-1𝛽 and TNF-𝛼 but not IL-6 was significantly inhibited by RGFM. Furthermore, RGFM water extract inhibited the phosphorylation of c-Jun N-terminal kinase (JNK). Conclusions : Taken together, these findings suggest that RGFM water extract has a protective effect on neuroinflammation through inhibition of JNK.

• The Korea Journal of Herbology
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• v.28 no.1
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• pp.43-50
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• 2013

Objectives : Hwanggeumjakyak-tang (huangqin shaoyao tang, HJT) has been used to treat acute enteritis in traditional oriental medicine. However, there has been a lack of studies regarding the effects of HJT on the inflammatory activities and effector inflammatory disease mechanism about macrophage before is not known. So we examined the effect of HJT water extract on pro-inflammatory mediators in lipopolysaccharide (LPS) - stimulated mouse macrophage, RAW 264.7 cells. Methods : Cells were treated with 2 ug/mL of LPS 1 h prior to the addition of HJT. Cell viability was measured by MTS assay. The production of nitric oxide (NO) was determined by reacting cultured medium with Griess reagent. The expression of cyclooxygenase-2 (COX-2), inducible NO synthase (iNOS) and mitogen-activated protein kinases (MAPKs) was investigated by Western blot, RT-PCR. The content of level of cytokines (prostaglandin (PG) $E_2$, interleukin (IL)-6, IL-12, Tumor necrosis factor-alpha (TNF-${\alpha}$) and monocyte chemoattractant protein-1 (MCP-1)) in media from LPS-stimulated Raw 264.7 cells was analyed by ELISA kit. Results : HJT inhibited the production of NO, $PGE_2$, IL-6 as well as the expressions of iNOS, COX-2 but did not inhibit the production of IL-12, TNF-${\alpha}$, MCP-1 in the murine macrophage, RAW 264.7 cells. HJT also had suppression effects of LPS-induced MAPKs activation Conclusion : These results suggest that HJT has an anti-inflammatory therapeutic potential, which may result from inhibition of MAPK phosphorylation, thereby decreasing the expression of pro-inflammatory genes.

• The Korea Journal of Herbology
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• v.33 no.5
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• pp.81-88
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• 2018

Objectives : The aim of this study was to investigate the protective effects of an aqueous extract from Taxillus chinensis (DC.) Danser (TCE) in Monosodium iodoacetate (MIA)-induced osteoarthritis (OA) rat model. Methods : Sprague Dawley male rats were divided into the following four groups (n=6 per group): Normal (saline control), MIA (MIA-induced OA with vehicle), TCE (MIA-induced with TCE treatment), and IM (MIA-induced with indomethacin treatment). Rats in which OA was induced by MIA were treated with TCE (200 mg/kg) or indomethacin (1 mg/kg) for 4 weeks. Weight-bearing on the hind legs and body weights were measured weekly. At the end of the experiment (3 weeks after MIA injection), serum aspartate aminotransferase and alanine aminotransferase levels were measured to assess the liver toxicity induced by TCE. Its effects on serum inflammatory cytokine levels and tissue histopathology were also evaluated. Results : TCE restored the hind limb weight-bearing distribution. Serum levels of Interleukin 6 (IL-6), Tumor necrosis factor alpha (TNF-${\alpha}$) and Leukotriene B4 (LTB4) were significantly higher in the MIA group than in the Normal group, but serum IL-6 levels were significantly lower in the TCE group. In the TCE group, the synovial membrane was protected in hematoxylin and eosin and Safranin-O staining, respectively. Conclusions : TCE recovered the hind paw weight bearing distribution, inhibited the production of inflammatory cytokine, and protected synovial tissue and cartilage in the OA rat model. Therefore, TCE appears to be an effective therapeutic agent for treating OA and OA-related symptoms.

• Journal of Korean Medicine Rehabilitation
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• v.32 no.3
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• pp.1-11
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• 2022

Objectives This study was designed to evaluate the healing effect of Cordyceps Militaris (CM) on collagen II-induced arthritis rats. Methods Sprague-Dawley rats were randomly divided into 6 groups (normal, control, positive control, CM with low/medium/high dosage each). Type II collagen mixed with complete Freund's adjuvant (with 1:1 v/v) was injected subcutaneously, and the mixture was injected in a same manner one week after the first injection to boost arthritis. Arthritis index, paw thickness and von Frey test were conducted to observe physical changes. hematoxylin and eosin (H&E) staining was performed to observe knee cartilage. The levels of messenger RNA (mRNA) expressions of interleukin (IL)-1𝛽, IL-6, tumor necrosis factor-alpha (TNF-𝛼) in spleen were assessed by real-time polymerase chain reaction. Results Rheumatoid arthritis is an autoimmune disease that occurs on multiple joints and can lead to temporary shape change of bones or organ failure in severe cases. Here, we aimed to determine the effect of CM extract on rheumatoid arthritis by measuring paw thickness, arthritis index, conducting von Frey test and H&E staining, and evaluating the level of IL-1𝛽, IL-6, TNF-𝛼. As a result, paw thickness, arthritis index significantly decreased in low concentration group, hind leg became less sensitive in all expermental groups. Also, histological analysis showed that the damage of knee cartilage was prevented in all experimental groups. The level of mRNA of IL-1𝛽, IL-6, and TNF-𝛼 in spleen was analyzed to decide the effectiveness of CM extract. IL-1𝛽 did not show significant change, but IL-6 and TNF-𝛼 showed significant decrease in at least one of the experimental groups. Conclusions CM showed protective effect on knee tissue destruction and improved the physical conditions of the leg involving arthritis. Also, it showed that CM has anti-inflammatory effect on specific cytokines inducing rheumatoid arthritis. In conclusion, this study demonstrated that the therapeutic potential of CM for the treatment rheumatoid arthritis, and set the foundation for the further studies.

• Journal of Ginseng Research
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• v.47 no.1
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• pp.97-105
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• 2023

Background: Hyperactivated airway mucosa cells overproduce mucin and cause severe breathing complications. Here, we aimed to identify the effects of saponins derived from Panax ginseng on inflammation and mucin overproduction. Methods: NCI-H292 cells were pre-incubated with 16 saponins derived from P. ginseng, and mucin overproduction was induced by treatment with phorbol 12-myristate 13-acetate (PMA). Mucin protein MUC5AC was quantified by enzyme-linked immunosorbent assay, and mRNA levels were analyzed using quantitative polymerase chain reaction (qPCR). Moreover, we performed a transcriptome analysis of PMA-treated NCI-H292 cells in the absence or presence of Rg5, and differential gene expression was confirmed using qPCR. Phosphorylation levels of signaling molecules, and the abundance of lipid droplets, were measured by western blotting, flow cytometry, and confocal microscopy. Results: Ginsenoside Rg5 effectively reduced MUC5AC secretion and decreased MUC5AC mRNA levels. A systematic functional network analysis revealed that Rg5 upregulated cholesterol and glycerolipid metabolism, resulting in the production of lipid droplets to clear reactive oxygen species (ROS), and modulated the mitogen-activated protein kinase and nuclear factor (NF)-kB signaling pathways to regulate inflammatory responses. Rg5 induced the accumulation of lipid droplets and decreased cellular ROS levels, and N-acetyl-ⳑ-cysteine, a ROS inhibitor, reduced MUC5AC secretion via Rg5. Furthermore, Rg5 hampered the phosphorylation of extracellular signal-regulated kinase and p38 proteins, affecting the NF-kB signaling pathway and pro-inflammatory responses. Conclusion: Rg5 alleviated inflammatory responses by reducing mucin secretion and promoting lipid droplet-mediated ROS clearance. Therefore, Rg5 may have potential as a therapeutic agent to alleviate respiratory disorders caused by hyperactivation of mucosa cells.

• 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.

• Journal of Ginseng Research
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• v.47 no.4
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• pp.515-523
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• 2023

Background: 20(S)-protopanaxadiol (PPD), one of the main components of ginseng, has anti-inflammatory, anti-estrogenic, and anti-tumor activities. It is known that activated hepatic stellate cells (HSCs) are the primary producers of extracellular matrix (ECM) in the liver, and the Wnt/β-catenin pathway participates in the activation of HSCs. We aimed to explore whether PPD inhibits liver fibrosis is associated with the Wnt/β-catenin pathway inactivation. Methods: The anti-fibrotic roles of PPD were examined both in vitro and in vivo. We also examined the levels of Wnt inhibitory factor 1 (WIF1), DNA methyltransferase 1 (DNMT1) and WIF1 methylation. Results: PPD obviously ameliorated liver fibrosis in carbon tetrachloride (CCl₄)-treated mice and reduced collagen deposition. PPD also suppressed the activation and proliferation of primary HSCs. Notably, PPD inhibited the Wnt/β-catenin pathway, reduced TCF activity, and increased P-β-catenin and GSK-3β levels. Interestingly, WIF1 was found to mediate the inactivation of the Wnt/β-catenin pathway in PPD-treated HSCs. WIF1 silencing suppressed the inhibitory effects of PPD on HSC activation and also restored α-SMA and type I collagen levels. The downregulation of WIF1 expression was associated with the methylation of its promoter. PPD induced WIF1 demethylation and restored WIF1 expression. Further experiments confirmed that DNMT1 overexpression blocked the effects of PPD on WIF1 expression and demethylation and enhanced HSC activation. Conclusion: PPD up-regulates WIF1 levels and impairs Wnt/β-catenin pathway activation via the downregulation of DNMT1-mediated WIF1 methylation, leading to HSC inactivation. Therefore, PPD may be a promising therapeutic drug for patients with liver fibrosis.

• Exercise Science
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• v.21 no.3
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• pp.289-298
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• 2012

In the present study, we investigated the effect of treadmill exercise on apoptotic neuronal cell death in the retinas of streptozotocin-induced diabetic rats. Twenty-eight male Sprague-Dawley rats were used for this study. The animals were divided into four groups(n = 7 in each group):(1) control group, (2) exercise group, (3) diabetes-induced group, (4) diabetes-induced and exercise group. Diabetes mellitus(DM) was induced by intraperitoneal injection of streptozotocin. The rats in the exercise groups were forced to run on the treadmill for 30 minutes once a day, five times per a week, during 12 weeks. In this study, a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) assay and western blot for the expressions of caspase-3, cytochrome c, Bax, and Bcl-2 in the retinas were conducted for the detection of apoptotic retinal cell death. The present results showed that the number of TUNEL-positive cells was increased in the retinas of the diabetic rats, whereas treadmill exercise suppressed this number. The expressions of pro-apoptotic factors caspase-3, cytochrome c, and Bax were enhanced and the expressions of anti-apoptotic factor Bcl-2 was decreased in the retinas of the diabetic rats. In contrast, treadmill exercise suppressed the expressions of caspase-3, cytochrome c, and Bax and increased the expression of Bcl-2. The present study demonstrated that treadmill exercise suppressed diabetes-induced apoptotic neuronal cell death in the retinas. Based on the present results, treadmill exercise may be effective therapeutic strategy for the alleviating complications of diabetes patients.

• Journal of Korean Neurosurgical Society
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• v.67 no.4
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• pp.418-430
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• 2024

Objective : Isoflurane, a widely used common inhalational anesthetic agent, can induce brain toxicity. The challenge lies in protecting neurologically compromised patients from neurotoxic anesthetics. Choline alfoscerate (L-α-Glycerophosphorylcholine, α-GPC) is recognized for its neuroprotective properties against oxidative stress and inflammation, but its optimal therapeutic window and indications are still under investigation. This study explores the impact of α-GPC on human astrocytes, the most abundant cells in the brain that protect against oxidative stress, under isoflurane exposure. Methods : This study was designed to examine changes in factors related to isoflurane-induced toxicity following α-GPC administration. Primary human astrocytes were pretreated with varying doses of α-GPC (ranging from 0.1 to 10.0 µM) for 24 hours prior to 2.5% isoflurane exposure. In vitro analysis of cell morphology, water-soluble tetrazolium salt-1 assay, quantitative real-time polymerase chain reaction, proteome profiler array, and transcriptome sequencing were conducted. Results : A significant morphological damage to human astrocytes was observed in the group that had been pretreated with 10.0 mM of α-GPC and exposed to 2.5% isoflurane. A decrease in cell viability was identified in the group pretreated with 10.0 µM of α-GPC and exposed to 2.5% isoflurane compared to the group exposed only to 2.5% isoflurane. Quantitative real-time polymerase chain reaction revealed that mRNA expression of heme-oxygenase 1 and hypoxia-inducible factor-1α, which were reduced by isoflurane, was further suppressed by 10.0 µM α-GPC pretreatment. The proteome profiler array demonstrated that α-GPC pretreatment influenced a variety of factors associated with apoptosis induced by oxidative stress. Additionally, transcriptome sequencing identified pathways significantly related to changes in isoflurane-induced toxicity caused by α-GPC pretreatment. Conclusion : The findings suggest that α-GPC pretreatment could potentially enhance the vulnerability of primary human astrocytes to isoflurane-induced toxicity by diminishing the expression of antioxidant factors, potentially leading to amplified cell damage.