• Proceedings of the Korean Society of Veterinary Clinics Conference
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• 2007.05a
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• pp.93-93
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• 2007

• CELLMED
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• v.2 no.4
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• pp.34.1-34.5
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• 2012

The present study aimed to determine the hepatoprotective activity of the chloroform extract of D. linearis leaves (CEDL) using the paracetamol (PCM)- and carbon tetrachloride ($CCl_4$)-induced liver injury models in rats. The rats received $dH_2O$ (negative control), 200 mg/kg of silymarin (positive control) or CEDL (50, 250 and 500 mg/kg) orally once daily for 7 days and then were subjected to the hepatotoxic induction on the $7^{th}$ day. The samples (i.e. blood and liver) were collected and underwent biochemical and microscopical analysis, respectively. From the data obtained, both inducers caused significant (p < 0.05) increase in the levels of AST and ALT when compared to the control group, which were significantly (p < 0.05) reduced by CEDL in a generally dose-dependent manner. These biochemical findings were supported by the histopathological analysis and histological scoring. In conclusion, CEDL possesses potential hepatoprotective activity, which could be associated with its flavonoid and tannin contents with the mechanisms of hepatoprotection linked to either its antioxidant or anti-inflammtory/immunomodulating activities. Further in-depth studies are required to identify the responsible bioactive compound.

• Biomedical Science Letters
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• v.20 no.4
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• pp.237-243
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• 2014

Triglyceride (TG) can cause death of macrophages and formation of foam cells thereby increasing inflammation in atherosclerotic plaques. Accumulation of cholesterol in macrophages is another critical event that promotes development of inflammatory cardiovascular diseases. Several proteins are known to transport intracellular cholesterol outside of the cell and these proteins are thought to be protective against atherosclerosis pathogenesis. It is unknown whether TG can affect cholesterol efflux in macrophages. In the current study, we examined mRNA expression levels of genes that promote efflux of cholesterol (ABCA1, ABCG1 and SR-B1). We found that TG treated THP-1 macrophages exhibited an increase in ABCG1 expression in a dose- and time-dependent manner. In contrast, the expression of ABCA1 and SR-B1 remained unchanged. To identify cell signaling pathways that participate in up-regulation of ABCG1, THP-1 macrophages were treated with various cell signaling inhibitors. We found that inhibition of the JNK and p38 MAPK pathway completely abrogated up-regulation of ABCG1 whereas inhibition of MEK1 further enhanced ABCG1 expression in TG treated THP-1 macrophages. Also, TG induced phosphorylation of JNK and p38 MAPK in THP-1 macrophages. These results suggest that TG may potentially influence cholesterol efflux in macrophages.

• Journal of Microbiology and Biotechnology
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• v.27 no.11
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• pp.2074-2074
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• 2017

• Biomolecules & Therapeutics
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• v.28 no.6
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• pp.527-536
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• 2020

Liver fibrosis constitutes a significant health problem worldwide due to its rapidly increasing prevalence and the absence of specific and effective treatments. Growing evidence suggests that apoptosis-signal regulating kinase 1 (ASK1) is activated in oxidative stress, which causes hepatic inflammation and apoptosis, leading to liver fibrogenesis through a mitogen-activated protein kinase (MAPK) downstream signals. In this study, we investigated whether selonsertib, a selective inhibitor of ASK1, shows therapeutic efficacy for liver fibrosis, and elucidated its mechanism of action in vivo and in vitro. As a result, selonsertib strongly suppressed the growth and proliferation of hepatic stellate cells (HSCs) and induced apoptosis by increasing Annexin V and TUNEL-positive cells. We also observed that selonsertib inhibited the ASK1/MAPK pathway, including p38 and c-Jun N-terminal kinase (JNK) in HSCs. Interestingly, dimethylnitrosamine (DMN)-induced liver fibrosis was significantly alleviated by selonsertib treatment in rats. Furthermore, selonsertib reduced collagen deposition and the expression of extracellular components such as α-smooth muscle actin (α-SMA), fibronectin, and collagen type I in vitro and in vivo. Taken together, selonsertib suppressed fibrotic response such as HSC proliferation and extracellular matrix components by blocking the ASK1/MAPK pathway. Therefore, we suggest that selonsertib may be an effective therapeutic drug for ameliorating liver fibrosis.

• Genomics & Informatics
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• v.21 no.2
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• pp.18.1-18.11
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• 2023

Immunologists have activated T cells in vitro using various stimulation methods, including phorbol myristate acetate (PMA)/ionomycin and αCD3/αCD28 agonistic antibodies. PMA stimulates protein kinase C, activating nuclear factor-κB, and ionomycin increases intracellular calcium levels, resulting in activation of nuclear factor of activated T cell. In contrast, αCD3/αCD28 agonistic antibodies activate T cells through ZAP-70, which phosphorylates linker for activation of T cell and SH2-domain-containing leukocyte protein of 76 kD. However, despite the use of these two different in vitro T cell activation methods for decades, the differential effects of chemical-based and antibody-based activation of primary human T cells have not yet been comprehensively described. Using single-cell RNA sequencing (scRNA-seq) technologies to analyze gene expression unbiasedly at the single-cell level, we compared the transcriptomic profiles of the non-physiological and physiological activation methods on human peripheral blood mononuclear cell-derived T cells from four independent donors. Remarkable transcriptomic differences in the expression of cytokines and their respective receptors were identified. We also identified activated CD4 T cell subsets (CD55⁺) enriched specifically by PMA/ionomycin activation. We believe this activated human T cell transcriptome atlas derived from two different activation methods will enhance our understanding, highlight the optimal use of these two in vitro T cell activation assays, and be applied as a reference standard when analyzing activated specific disease-originated T cells through scRNA-seq.

• Journal of Ginseng Research
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• v.48 no.1
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• pp.59-67
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• 2024

Background: Alzheimer's disease (AD) has memory impairment associated with aggregation of amyloid plaques and neurofibrillary tangles in the brain. Although anti-amyloid β (Aβ) protein antibody and chemical drugs can be prescribed in the clinic, they show adverse effects or low effectiveness. Therefore, the development of a new drug is necessarily needed. We focused on the cognitive function of Panax ginseng and tried to find active ingredient(s). We isolated panaxcerol D, a kind of glycosyl glyceride, from the non-saponin fraction of P. ginseng extract. Methods: We explored effects of acute or sub-chronic administration of panaxcerol D on cognitive function in scopolamine- or Aβ_25-35 peptide-treated mice measured by several behavioral tests. After behavioral tests, we tried to unveil the underlying mechanism of panaxcerol D on its cognitive function by Western blotting. Results: We found that pananxcerol D reversed short-term, long-term and object recognition memory impairments. The decreased extracellular signal-regulated kinases (ERK) or Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) in scopolamine-treated mice was normalized by acute administration of panaxcerol D. Glial fibrillary acidic protein (GFAP), caspase 3, NF-kB p65, synaptophysin and brainderived neurotrophic factor (BDNF) expression levels in Aβ_25-35 peptide-treated mice were modulated by sub-chronic administration of panaxcerol D. Conclusion: Pananxcerol D could improve memory impairments caused by cholinergic blockade or Aβ accumulation through increased phosphorylation level of ERK or its anti-inflammatory effect. Thus, panaxcerol D as one of non-saponin compounds could be used as an active ingredient of P. ginseng for improving cognitive function.

• BMB Reports
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• v.42 no.2
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• pp.81-85
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• 2009

Early and accurate detection of drug resistant Mycobacterium tuberculosis can improve both the treatment outcome and public health control of tuberculosis. A number of molecular-based techniques have been developed including ones using probe molecules that target drug resistance-related mutations. Although these techniques are highly specific and sensitive, mixed signals can be obtained when the drug resistant isolates are mixed with drug susceptible isolates. In order to overcome this problem, we developed a new drug susceptibility test (DST) for one of the most effective anti-tuberculosis drug, isoniazid. This technique employed a microplate hybridization assay that quantified signals from each probe molecule, and was evaluated using clinical isolates. The evaluation analysis clearly showed that the microplate hybridization assay was an accurate and rapid method that overcame the limitations of DST based on conventional molecular techniques.

• Biomolecules & Therapeutics
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• v.21 no.3
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• pp.222-228
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• 2013

Although the role of ${\alpha}$-synuclein aggregation on Parkinson's disease is relatively well known, the physiological role and the regulatory mechanism governing the expression of ${\alpha}$-synuclein are unclear yet. We recently reported that ${\alpha}$-synuclein is expressed and secreted from cultured astrocytes. In this study, we investigated the effect of valproic acid (VPA), which has been suggested to provide neuroprotection by increasing ${\alpha}$-synuclein in neuron, on ${\alpha}$-synuclein expression in rat primary astrocytes. VPA concentration-dependently increased the protein expression level of ${\alpha}$-synuclein in cultured rat primary astrocytes with concomitant increase in mRNA expression level. Likewise, the level of secreted ${\alpha}$-synuclein was also increased by VPA. VPA increased the phosphorylation of Erk1/2 and JNK and pretreatment of a JNK inhibitor SP600125 prevented the VPA-induced increase in ${\alpha}$-synuclein. Whether the increased ${\alpha}$-synuclein in astrocytes is involved in the reported neuroprotective effects of VPA awaits further investigation.

• Biomedical Science Letters
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• v.28 no.4
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• pp.307-311
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• 2022

The extract of EA lacks studies showing its efficacy other than that it contains caffeic acid, an active compound that has antioxidant and neuroprotective effects on nerve cells. Therefore, in this study, we attempted to determine the effectiveness of EA extraction. In this study, we performed a DPPH assay to determine the antioxidant potential of EA. And then, the cytotoxic concentration of EA in HaCaT keratinocytes was determined, and the antioxidant effect was determined by measuring the malondialdehyde (MDA). The results of DPPH, a chemical antioxidant assay, clearly demonstrated the antioxidant capacity of EA extracted with distilled water. In addition, cell-based assays provide useful information on the protective effect of EA on oxidative stress-induced apoptosis.