• The Journal of Pediatrics of Korean Medicine
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• v.20 no.2
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• pp.177-196
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• 2006

Objective : This experimental study was designed to determine the effects of BPT on obesity in vivo and in vitro. Methods : in vitro, BPTn extracts of various concentration(50, 100, 200 ${\mu}g/m{\ell}$) were added in 3T3-L1 cell. Adipocyte differentiation was measured by Oil Red O staining and Morphological examination. The expression of $C/EBP{\alpha}$ and $PPAR{\gamma}$ receptor was measured by western blot assay and RT-PCR in vivo, Rats were orally administered BPT daily for consecutive four weeks before poloxamer-407 induced hyperlipidemic state. The rats were sacrificed 24 hrs later for poloxamer-407 treated and then serum triglyceride, total cholesterol were measured ; Rats were orally administered BPT daily for consecutive four weeks before triton WR-1339 induced hyperlipidemic state. The rats were sacrificed 40 hrs later for triton WR-1339 treated and then serum triglyceride, total cholesterol were measured ; Rats with obesity were induced by the high fat-diet for six weeks and then serum triglyceride, total cholesterol, LDL-cholesterol, triglyceride, HDL-cholesterol, hydroxy radical, superoxide dismuatse activity were measured. Results : In vitro, The 3T3-L1 cells' differentiation was significantly decreased by BPT. The expression of $C/EBP{\alpha}$ and $C/EBP{\beta}$ was decreased by BPT. In vivo, BPT significantly reduced serum triglyceride, total cholesterol contents in poloxamer-407 treated rat. BPT significantly reduced serum triglyceride contents in Triton WR-1339 treated rat. Total cholesterol also reduced but did not show a significant change. BPT significantly reduced body weight gain of rat and adipose tissue mass of rats and serum triglyceride, LDL-cholesterol contents and significantly increased HDL-cholesterol, HTR(HDL-cholesterol/Total-cholesterol) in rats with obesity induced by the high fat-diet. BPT reduced blood lipid peroxide, hydroxy radical and increased superoxide dismuatse(SOD) activity.

• Journal of Applied Biological Chemistry
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• v.66
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• pp.204-212
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• 2023

Whitening is inhibitory activity of the melanin synthesis of melanocytes. Recently, whitening materials have been developed on natural materials because of its side effects on skin. Figs (Ficus Carica L.) is a fruit belonging to the Moraceae family and whitening activity was reported in focusing on the fig's stem and leaf components, but whitening activity of the figs fruit was not known. Thus, in this study, we tried to observe its anti-melanogenesis as well as antioxidant and anti-inflammation. The radical scavenging activity of figs fruits extract (FFE) was observed as the level of 34.52±1.98%/60.71±1.26% compared to the control in the its maximum concentration in the DPPH/ABTS assay. Cytotoxicity of FFE was observed at 10% concentration by CCK8 assay, so the maximum concentration was set at 5% and applied to all experiments. FFE concentration dependently decreased NO production associated with inducible nitric oxide synthase, cyclooxygenase-2, interleukin-6 and tumor necrosis factor-α gene expression, these strongly suggesting anti-inflammatory activity. In melanin contents assay, FFE significantly down-regulated melanin production in α-MSH-stimulated B16F10 cell as well as tyrosinase inhibition in vitro. In addition, FFE decreased the Microphthalmia-associated transcription factor (MITF) mRNA expression about 94.34% compared to the α-MSH treatment group in RT-PCR. Finally, FFE significantly reduced the MITF, cAMP response element-binding protein and tyrosinase protein expression in the α-MSH stimulated B16F10 cell. Through these results, we found that FFE can not only directly inhibit tyrosinase enzyme activity but also suppress melanogenesis through regulation of MITF gene expression in α-MSH signal transduction.

• Macromolecular Research
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• v.12 no.1
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• pp.46-52
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• 2004

In a continuation of our previous studies on blood compatibility profiles of anion-substituted poly(vinyl alcohol) (PVA) membranes, in which hydroxyl groups have been replaced with carboxymethyl (C-PVA) and sulfonyl groups (S-PVA), we have studied the activation of complement components and the changes in white cell and platelet count in vitro and compared them with those of unmodified PVA, Cuprophane, and low-density polyethylene. Complement activation of fluid phase components, C3a, Bb, iC3b, and SC5b-9, and of bound phases, C3c, C3d, and SC5b-9, were assessed by enzyme-linked immunosorbent assay (ELISA) and immunoblot, respectively. The changes in the number of white cells and platelets following complement activation were counted using a Coulter counter. C-PVA and S-PVA activated C3 to a lesser extent than did PVA, which we attribute to the diminished level of surface nucleophiles of the samples. In addition, C- and S-PVA exhibit increased inhibition of Bb production, resulting in a decrease in the extent of C5 activation. Consequently, because of the reduced activation of C3 and C5, C- and S-PVA samples cause marked decreases in the SC5b-9 levels in plasma. We also found that the negatively charged sulfonate and carboxylate groups of the samples cause a greater extent of adsorbtion of the positively charged anaphylatoxins, C3a and C5a, because of strong electrostatic attraction, which in turn provides an inhibition of chemotaxis and activation of leukocytes. The ability to inhibit complement production, together with the binding ability of anaphylatoxins of the C- and S-PVA samples, leads to a prominent decrease in lysis of leukocytes as well as activation of platelets.

• Nutrition Research and Practice
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• v.17 no.1
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• pp.164-173
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• 2023

BACKGROUND/OBJECTIVES: Hyperglycemia is a major cause of diabetes and diabetesrelated diseases. Sodium butyrate (NaB) is a short-chain fatty acid derivative that produces dietary fiber by anaerobic bacterial fermentation in the large intestine and occurs in foods, such as Parmesan cheese and butter. Butyrate has been shown to prevent obesity, improve insulin sensitivity, and ameliorate dyslipidemia in diet-induced obese mice. Therefore, this study examined the effects and mechanism of NaB on the secretion of inflammatory cytokines induced by high glucose (HG) in THP-1 cells. MATERIALS/METHODS: THP-1 cells were used as an in vitro model for HG-induced inflammation. The cells were cultured under normal glycemic or hyperglycemic conditions with or without NaB (0-25 μM). Western blotting and quantitative polymerase chain reaction were used to evaluate the protein and mRNA levels of nuclear factor-κB (NF-κB), interleukin-6, tumor necrosis factor-α, acetylated p65, acetyl CREB-binding protein/p300 (CBP/p300), and p300 using THP-1 cells. Histone acetyltransferase (HAT), histone deacetylase (HDAC), and pro-inflammatory cytokine secretion activity were analyzed using an enzyme-linked immunosorbent assay. RESULTS: HG significantly upregulated histone acetylation, acetylation levels of p300, NF-κB activation, and inflammatory cytokine release in THP-1 cells. Conversely, the NaB treatment reduced cytokine release and NF-κB activation in HG-treated cells. It also significantly reduced p65 acetylation, CBP/p300 HAT activity, and CBP/p300 gene expression. In addition, NaB decreased the interaction of p300 in acetylated NF-κB and TNF-α. CONCLUSIONS: These results suggest that NaB suppresses HG-induced inflammatory cytokine production through HAT/HDAC regulation in monocytes. NaB has the potential for preventing and treating diabetes and its related complications.

• Journal of Microbiology and Biotechnology
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• v.18 no.5
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• pp.837-844
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• 2008

Glucose (xylose) isomerases from Streptomyces sp. have been used for the production of high fructose corn syrup for industrial purposes. An 11-kb DNA fragment containing the xyl gene cluster was isolated from Streptomyces lividans TK24 and its nucleotide sequences were analyzed. It was found that the xyl gene cluster contained a putative transcriptional repressor (xylR), xylulokinase (xylB), and xylose isomerase (xylA) genes. The transcriptional directions of the xylB and xylA genes were divergent, which is consistent to those found in other streptomycetes. A gene encoding XylR was located downstream of the xylB gene in the same direction, and its mutant strain produced xylose isomerase regardless of xylose in the media. The enzyme expression level in the mutant was 4.6 times higher than that in the parent strain under xylose-induced condition. Even in the absence of xylose, the mutant strain produce over 60% of enzyme compared with the xylose-induced condition. Gel mobility shift assay showed that XylR was able to bind to the putative xyl promoter, and its binding was inhibited by the addition of xylose in vitro. This result suggested that XylR acts as a repressor in the S. lividans xylose operon.

• Biomolecules & Therapeutics
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• v.30 no.6
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• pp.520-528
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• 2022

Mast cells are an effector cell that plays a pivotal role in type I hypersensitive immune responses. Mast cells exist in connective tissues, such as skin and mucosal tissue, and contain granules which contain bioactive substances such as histamine and heparin in cells. The granules of mast cells are secreted by antigen stimulation to cause the type I allergic hypersensitivity. In addition, stimulated by antigen, mast cells synthesize and secrete various eicosanoids and cytokines. While AT9283 is known to have anticancer effects, the therapeutic effect of AT9283 on allergic disorders is completely unknown. In this study, it was found that AT9283 reversibly inhibited antigen-IgE binding-induced degranulation in mast cells (IC₅₀, approx. 0.58 μM) and suppressed the secretion of the inflammatory cytokines IL-4 (IC₅₀, approx. 0.09 μM) and TNF-α (IC₅₀, approx. 0.19 μM). For a mechanism of mast cell inhibition, while not inhibiting Syk phosphorylation, AT9283 suppressed the activation of LAT, a downstream substrate protein of Syk, in a dose-dependent manner. As expected, AT9283 also inhibited the activation of PLCγ1 and Akt, downstream signaling molecules of Syk/LAT, and MAP kinases such as JNK, Erk1/2, and P38. In an in vitro protein tyrosine kinase assay, AT9283 directly inhibited Syk activity. Next, AT9283 dose-dependently inhibited passive cutaneous anaphylaxis (PCA), an IgE-mediated allergic acute response, in mice (ED50, approx. 34 mg/kg, p.o.). These findings suggest that AT9283 has potential to use as a new drug for alleviating the symptoms of IgE-mediated allergic disorders.

• Microbiology and Biotechnology Letters
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• v.33 no.4
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• pp.255-259
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• 2005

IgE-dependent histamine-releasing factor (HRF) is found extracellularly to regulate the degranulation process of histamine in mast cells and basophils and known to play a predominant role in the pathogenesis of chronic allergic disease. HRF has been also identified in the intracellular region of the cell. Previously, we reported that HRF interacts with the 3rd cytoplasmic domain of the alpha subunit of Na,K-ATPase. To understand the molecular mechanism of the regulation of Na, K-ATPase activity by HRF, we investigated the interaction between HRF and TPI since TPI was obtained as HRF-interacting protein in HeLa cDNA library, using yeast two hybrid screening. Domain mapping study of the interaction between HRF and TPI revealed that the C-terminal region of the residue 156-249 of TPI is involved in the interaction with HRF. The interaction between HRF and TPI was confirmed by immunoprecipitation from HeLa cell extracts. Our results suggest that TPI is a HRF-binding protein and the interaction between HRF and TPI nay thus affect Na, K-ATPase activity.

• Journal of Microbiology and Biotechnology
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• v.26 no.6
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• pp.1132-1139
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• 2016

Brucellosis is a zoonotic disease caused by Brucella, a genus of gram-negative bacteria. Cytokines have key roles in the activation of innate and acquired immunities. Despite several research attempts to reveal the immune responses, the mechanism of Brucella infection remains unclear. Therefore, immune responses were analyzed in mice immunized with nine recombinant proteins. Cytokine production profiles were analyzed in the RAW 264.7 cells and naive splenocytes after stimulation with three recombinant proteins, metal-dependent hydrolase (r0628), bacterioferritin (rBfr), and thiamine transporter substrate-binding protein (rTbpA). Immune responses were analyzed by ELISA and ELISpot assay after immunization with proteins in mice. The production levels of NO, TNF-α, and IL-6 were time-dependently increased after having been stimulated with proteins in the RAW 264.7 cells. In naive splenocytes, the production of IFN-γ and IL-2 was increased after stimulation with the proteins. It was concluded that two recombinant proteins, r0628 and rTbpA, showed strong immunogenicity that was induced with Th1-related cytokines IFN-γ, IL-2, and TNF-α more than Th2-related cytokines IL-6, IL-4, and IL-5 in vitro. Conversely, a humoral immune response was activated by increasing the number of antigen-secreting cells specifically. Furthermore, these could be candidate diagnosis antigens for better understanding of brucellosis.

• Korean Circulation Journal
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• v.53 no.3
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• pp.151-167
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• 2023

Background and Objectives: Acute myocardial infarction (AMI) often occurs suddenly and leads to fatal consequences. Ferroptosis is closely related to the progression of AMI. However, the specific mechanism of ferroptosis in AMI remains unclear. Methods: We constructed a cell model of AMI using AC16 cells under oxygen and glucose deprivation (OGD) conditions and a mice model of AMI using the left anterior descending (LAD) ligation. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide was employed to determine cell viability. The levels of lactate dehydrogenase, creatine kinase, reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and iron were measured using corresponding kits. Dual luciferase reporter gene assay, RNA-binding protein immunoprecipitation, and RNA pull-down were performed to validate the correlations among AC005332.7, miR-331-3p, and cyclin D2 (CCND2). Hematoxylin and eosin staining was employed to evaluate myocardial damage. Results: AC005332.7 and CCND2 were lowly expressed, while miR-331-3p was highly expressed in vivo and in vitro models of AMI. AC005332.7 sufficiency reduced ROS, MDA, iron, and ACSL4 while boosting the GSH and GPX4, indicating that AC005332.7 sufficiency impeded ferroptosis to improve cardiomyocyte injury in AMI. Mechanistically, AC005332.7 interacted with miR-331-3p, and miR-331-3p targeted CCND2. Additionally, miR-331-3p overexpression or CCND2 depletion abolished the suppressive impact of AC005332.7 on ferroptosis in OGD-induced AC16 cells. Moreover, AC005332.7 overexpression suppressed ferroptosis in mice models of AMI. Conclusions: AC005332.7 suppressed ferroptosis in OGD-induced AC16 cells and LAD ligation-operated mice through modulating miR-331-3p/CCND2 axis, thereby mitigating the cardiomyocyte injury in AMI, which proposed novel targets for AMI treatment.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.1
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• pp.289-294
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• 2012

Background: Myofibroblasts play an important role in the development of oral submucous fibrosis (OSF). In the current study, we investigate the effect of curcumin on growth and apoptosis of myofibroblasts derived from human oral mucosa. Methods: Myofibroblasts were generated by incubating fibroblasts, obtained from human oral mucosa, with transforming growth factor-${\beta}1$ (TGF-${\beta}1$). MTT, PI staining, and FACS assays were used to investigate curcumin's effect on proliferation and cell cycle of fibroblasts and myofibroblasts. Annexin V/PI binding and FACS assays were used to examine apoptosis of myofibroblasts, Western blotting to determine the levels of Bcl-2 and Bax, and enzyme-linked immunosorbant assay was employed to examine the levels of collagen type I and III in the supernatants of myofibroblasts. Results: Curcumin inhibits proliferation of fibroblasts and myofibroblasts; it also disturbs the cell cycle, induces apoptosis and decreases the generation of collagen type I and III in myofibroblasts, which are more sensitive to its effects than fibroblasts. Curcumin induces apoptosis in myofibroblasts by down-regulating the Bcl-2/ Bax ratio. Conclusion: Our results demonstrate the antifibrotic effect of curcumin in vitro. It may therefore be a candidate for the treatment of OSF.