• Molecules and Cells
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• v.40 no.7
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• pp.457-465
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• 2017

Streptozotocin (STZ)-induced murine models of type 1 diabetes have been used to examine ER stress during pancreatic ${\beta}$-cell apoptosis, as this ER stress plays important roles in the pathogenesis and development of the disease. However, the mechanisms linking type 1 diabetes to the ER stress-modulating anti-diabetic signaling pathway remain to be addressed, though it was recently established that ERK5 (Extracellular-signal-regulated kinase 5) contributes to the pathogeneses of diabetic complications. This study was undertaken to explore the mechanism whereby ERK5 inhibition instigates pancreatic ${\beta}$-cell apoptosis via an ER stress-dependent signaling pathway. STZ-induced diabetic WT and CHOP deficient mice were i.p. injected every 2 days for 6 days under BIX02189 (a specific ERK5 inhibitor) treatment in order to evaluate the role of ERK5. Hyperglycemia was exacerbated by co-treating C57BL/6J mice with STZ and BIX02189 as compared with mice administered with STZ alone. In addition, immunoblotting data revealed that ERK5 inhibition activated the unfolded protein response pathway accompanying apoptotic events, such as, PARP-1 and caspase-3 cleavage. Interestingly, ERK5 inhibition-induced exacerbation of pancreatic ${\beta}$-cell apoptosis was inhibited in CHOP deficient mice. Moreover, transduction of adenovirus encoding an active mutant form of $MEK5{\alpha}$, an upstream kinase of ERK5, inhibited STZ-induced unfolded protein responses and ${\beta}$-cell apoptosis. These results suggest that ERK5 protects against STZ-induced pancreatic ${\beta}$-cell apoptosis and hyperglycemia by interrupting the ER stress-mediated apoptotic pathway.

• Journal of Applied Biological Chemistry
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• v.60 no.1
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• pp.13-17
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• 2017

To develop a new functional agent for cosmetics, we investigated the anti-aging activities in fibroblasts of casuarictin. The anti-aging effect of casuarictin in CCD-986sk cell was as follows: it inhibited ROS expression increased by Ultraviolet B and suppressed pro-collagen expression. Also, casuarictin had inhibited Matrix metalloproteinase-1 expression. Therefore, the results suggested that casuarictin has considerable potential as a cosmetics ingredient with a anti-aging effect.

• The Korea Journal of Herbology
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• v.34 no.6
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• pp.109-115
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• 2019

Objective : Herbal medicinal mixture (JMB) are consisted of Caryophylli Flos, Aucklandiae Radix, and Angelicae Dahuricae Radix. Each of these herbal medicines has studied on anti-aging effect in vitro. So this study was conducted to investigate efficacy and potency of JMB extract on dermal anti-aging and whitening. Methods : The JMB was extracted at room temperature by 80% ethanol. Collagenase and elastase inhibition activity in JMB ethanol extract were determined at 10, 50, 100, 500, 1000 mg/ml concentrations by colorimetric method. The toxic range of JMB ethanol extract was evaluated using MTT assay. Also, The inhibitory effect of JMB ethanol extract on tyrosinase activity and melanin contents in mouse melanoma cell line (B16F10 cell) was identified at 50, 100, 200 ㎍/㎖ levels by spectrometric assay. In each analysis, EGCG (epigallocatechin gallate) and Kojic acid were used as positive controls, respectively. Results : The elastase and collagenase inhibitory activity of JMB ethanol extract increased dose dependently. Also, The MTT assay showed that JMB, up to 400 ㎍/㎖ concentration, exhibited no toxic effect to the B16F10 cell. And following the JMB ethanol extract treat, cellular melanin contents and tyrosinase activity were dose-dependently decreased compared to those of control. Conclusion : These results suggest that JMB ethanol extract has effects to inhibitory activity on dermal wrinkle enzyme and melanogenesis. Therefore, JMB has applicable benefits for development of materials or products to have whitening and anti-aging functions on skin.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2002.07a
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• pp.406-409
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• 2002

The primary insulation system used in an oil-filled transformer is Kraft paper, wood, porcelain and, of course, oil. Modern transformers use paper that is chemically treated to improve its tensile strength properties and resistance to aging caused by immersion in oil. These insulation papers are mainly aged to thermal stress. Over the course of the insulation paper and oil's life it is exposed to high temperatures, oxygen and water. Its interaction with the steel of the tank and core plus the copper and aluminium of the windings will eventually cause the chemical properties of the oil to decay. High temperature have an effect on mechanical strength of cellulous paper using the layer insulation. We made two aging cell in which thermal aging tests of insulation papers and mineral oil are conducted. It is measured dielectric strength, number of acid, moisture, etc. of insulation paper and oil aged in the aging cells.

• BMB Reports
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• v.46 no.9
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• pp.429-438
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• 2013

Aging is the strongest risk factor for cancer development, suggesting that molecular crosstalks between aging and tumorigenesis exist in many cellular pathways. Recently, Sirtuins (Sirt1-7), the mammalian homologues of aging-related $sir2{\alpha}$ in yeast, have been shown to modulate several major cellular pathways, such as DNA repair, inflammation, metabolism, cell death, and proliferation in response to diverse stresses, and may serve as a possible molecular link between aging and tumorignenesis. In addition, growing evidence suggests that sirtuins are directly implicated in the development of cancer, and they can act as either a tumor suppressor or promoter, depending on the cellular context and tumor types. While the functions of Sirt1 in tumorigenesis have been reported and reviewed in many studies, the connection between sirtuins 2-7 and the development of cancer is less established. Thus, this review will present the recent updates on the emerging roles of Sirt2-7 members in carcinogenesis.

• Journal of Microbiology and Biotechnology
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• v.33 no.5
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• pp.680-686
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• 2023

Aging is a complex series of multi-organ processes that occur in various organisms. As such, an in vivo study using an animal model of aging is necessary to define its exact mechanisms and identify anti-aging substances. Using Drosophila as an in vivo model system, we identified Crataegus pinnatifida extract (CPE) as a novel anti-aging substance. Regardless of sex, Drosophila treated with CPE showed a significantly increased lifespan compared to those without CPE. In this study, we also evaluated the involvement of CPE in aging-related biochemical pathways, including TOR, stem cell generation, and antioxidative effects, and found that the representative genes of each pathway were induced by CPE administration. CPE administration did not result in significant differences in fecundity, locomotion, feeding amount, or TAG level. These conclusions suggest that CPE is a good candidate as an anti-aging food substance capable of promoting a healthy lifespan.

• BMB Reports
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• v.52 no.6
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• pp.403-408
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• 2019

Dorsoventral patterning of body axis in vertebrate embryo is tightly controlled by a complex regulatory network of transcription factors. Ventx1.1 is known as a transcriptional repressor to inhibit dorsal mesoderm formation and neural differentiation in Xenopus. In an attempt to identify, using chromatin immunoprecipitation (ChIP)-Seq, genome-wide binding pattern of Ventx1.1 in Xenopus gastrulae, we observed that Ventx1.1 associates with its own 5'-flanking sequence. In this study, we present evidence that Ventx1.1 binds a cis-acting Ventx1.1 response element (VRE) in its own promoter, leading to repression of its own transcription. Site-directed mutagenesis of the VRE in the Ventx1.1 promoter significantly abrogated this inhibitory autoregulation of Ventx1.1 transcription. Notably, Ventx1.1 and Xcad2, an activator of Ventx1.1 transcription, competitively co-occupied the VRE in the Ventx1.1 promoter. In support of this, mutation of the VRE down-regulated basal and Xcad2-induced levels of Ventx1.1 promoter activity. In addition, overexpression of Ventx1.1 prevented Xcad2 from binding to the Ventx1.1 promoter, and vice versa. Taken together, these results suggest that Ventx1.1 negatively regulates its own transcription in competition with Xcad2, thereby fine-tuning its own expression levels during dorsoventral patterning of Xenopus early embryo.

• The Journal of the Korean dental association
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• v.11 no.5
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• pp.321-323
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• 1973

The auther observed the aging of oral epithelium in gingiva of edentulous jaw. The observed staning methods were PAS reaction of the epithelivm of the gingive were increased in aging group, the basal prickle and granulor cell layer presented a strong reaction. The collagenous fiber in subepithelical layer was, quantitalively inrcred accouding to aging.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.5
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• pp.299-304
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• 2010

Losartan is a selective angiotensin II (Ang II) type 1 ($AT_1$) receptor antagonist which inhibits vascular smooth muscle cells (VSMCs) contraction and proliferation. We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. VSMCs were treated with various concentrations of losartan. AMPK activation was measured by Western blot analysis and cell proliferation was measured by MTT assay and flowcytometry. Losartan dose- and time-dependently increased the phosphorylation of AMPK and its downstream target, acetyl-CoA carboxylase (ACC) in VSMCs. Losartan also significantly decreased the Ang II- or 15% FBS-induced VSMC proliferation by inhibiting the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E. Compound C, a specific inhibitor of AMPK, or AMPK siRNA blocked the losartan-induced inhibition of cell proliferation and the $G_0/G_1$ cell cycle arrest. These data suggest that losartan-induced AMPK activation might attenuate Ang II-induced VSMC proliferation through the inhibition of cell cycle progression.

• BMB Reports
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• v.54 no.5
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• pp.278-283
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• 2021

Our understanding of the differential effects between specific omega-3 fatty acids is incomplete. Here, we aimed to evaluate the effects of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on T-helper type 1 (Th1) cell responses and identify the pathways associated with these responses. Naïve CD4⁺ T cells were co-cultured with bone marrow-derived dendritic cells (DCs) in the presence or absence of palmitate (PA), DHA, or EPA. DHA or EPA treatment lowered the number of differentiated IFN-γ-positive cells and inhibited the secretion of IFN-γ, whereas only DHA increased IL-2 and reduced TNF-α secretion. There was reduced expression of MHC II on DCs after DHA or EPA treatment. In the DC-independent model, DHA and EPA reduced Th1 cell differentiation and lowered the cell number. DHA and EPA markedly inhibited IFN-γ secretion, while only EPA reduced TNF-α secretion. Microarray analysis identified pathways involved in inflammation, immunity, metabolism, and cell proliferation. Moreover, DHA and EPA inhibited Th1 cells through the regulation of diverse pathways and genes, including Igf1 and Cpt1a. Our results showed that DHA and EPA had largely comparable inhibitory effects on Th1 cell differentiation. However, each of the fatty acids also had distinct effects on specific cytokine secretion, particularly according to the presence of DCs.