• Korean Journal of Chemical Engineering
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• v.35 no.12
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• pp.2403-2412
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• 2018

The present study was aimed at evaluating the effect of variable sodium carbonate ($Na_2CO_3$) loading during wet air oxidation (WAO) pretreatment of rice straw in reducing biomass recalcitrance. The research study was intended to increase the cellulose recovery, hemicellulose solubilization, lignin removal in the solid fraction and limiting the generation of inhibitors in the liquid fraction while reducing the chemical input. The operating condition of $169^{\circ}C$, 4 bar, 18 min and 6.5 g/L $Na_2CO_3$ loading resulted in maximum cellulose recovery of 82.07% and hemicellulose solubilization and lignin removal of 85.43% and 65.42%, respectively, with a total phenolic content of 0.36 g/L in the liquid fraction. The crystallinity index increased from 47.69 to 51.25 along with enzymatic digestibility with an increase in $Na_2CO_3$ loading from 0 to 6.5 g/L as a result of removal of barriers for saccharification via effective cleavage of ether and ester bonds cross-linking the carbohydrates and lignin as indicated by FT-IR spectroscopy. A further increase in the $Na_2CO_3$ loading to 9.5 g/L did not significantly increase the sugar release. Thus, it was concluded that 6.5 g/L $Na_2CO_3$ during WAO is sufficient to increase the delignification and deacetylation, leading to significant changes in apparent cellulose crystallinity inter alia improvement in cellulose accessibility and digestibility of rice straw.

• BMB Reports
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• v.54 no.10
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• pp.534-539
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• 2021

IL-10⁺ regulatory B (Breg) cells play a vital role in regulating the immune responses in experimental autoimmune encephalomyelitis, colitis, and contact hypersensitivity (CHS). Several stimulants such as lipopolysaccharide (LPS), CD40 ligand, and IL-21 spur the activation and maturation of IL-10⁺ Breg cells, while the epigenetic mechanism for the IL-10 expression remains largely unknown. It is well accepted that the histone acetylation/deacetylation is an important mechanism that regulates the expression of IL-10. We found that entinostat, an HDAC inhibitor, stimulated the induction of IL-10⁺ Breg cells by LPS in vitro and the formation of IL-10⁺ Breg cells to suppress CHS in vivo. We further demonstrated that entinostat inhibited HDAC1 from binding to the proximal region of the IL-10 expression promoter in splenic B cells, followed by an increase in the binding of NF-κB p65, eventually enhancing the expression of IL-10 in Breg cells.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2003.10a
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• pp.181-181
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• 2003

We have studied the mechanism of action of TCDD on CYP1A1 promoter activity in both Hepa Ⅰ and MCF-7 cells using transient transfection system with p1A1-Luc reporter gene. When HDAC inhibitors, such as trichostatin A, HC toxin and a novel HDAC inhibitor, IN2001 were cotreated with TCDD to the cells transfected with plAt-Luc reporter gene, the basal promoter activity of CYP1A1 was increased by HBAC inhibitors. Also, in MCF-7 human breast cancer cells, HDAC inhibitors, such as IN2001 and trichostatin A increased the basal activity of CYP1A1 promoter but TCDD stimulated CYP1A1 promoter activity was not changed by HDAC inhibitors. And, in stably-transfected Hepa Ⅰ cells with p1A1-Luc, HDAC inhibitors increased the basal promoter activity only Also, we have investigated the effects of HDAC inhibitors on the human breast and prostate cancer cells in terms of cell proliferation and apoptosis based on SRB assay. IN2001 as well as trichostatin A inhibited the MCF-7, MDA-MB-231, MDA-MB-468, T47D, ZR75-1, PC3 cell growth dose-dependently. The growth inhibition of these cells with HDAC inhibitors was associated with profound morphological change, which suggests the HDAC inhibitors induced apoptosis of cells. The result of cell cycle analysis after 24h exposure of IN2001 showed G2/M cell cycle arrest in MCF-7 cells and apoptosis in T47D and MDA-MB-231 cells.

• Korean Circulation Journal
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• v.54 no.4
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• pp.172-186
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• 2024

Background and Objectives: Long-term pathological myocardial hypertrophy (MH) seriously affects the normal function of the heart. Dronedarone was reported to attenuate left ventricular hypertrophy of mice. However, the molecular regulatory mechanism of dronedarone in MH is unclear. Methods: Angiotensin II (Ang II) was used to induce cell hypertrophy of H9C2 cells. Transverse aortic constriction (TAC) surgery was performed to establish a rat model of MH. Cell size was evaluated using crystal violet staining and rhodamine phalloidin staining. Reverse transcription quantitative polymerase chain reaction and western blot were performed to detect the mRNA and protein expressions of genes. JASPAR and luciferase activity were conducted to predict and validate interaction between forkhead box O3 (FOXO3) and protein kinase inhibitor alpha (PKIA) promoter. Results: Ang II treatment induced cell hypertrophy and inhibited sirtuin 1 (SIRT1) expression, which were reversed by dronedarone. SIRT1 overexpression or PKIA overexpression enhanced dronedarone-mediated suppression of cell hypertrophy in Ang II-induced H9C2 cells. Mechanistically, SIRT1 elevated FOXO3 expression through SIRT1- mediated deacetylation of FOXO3 and FOXO3 upregulated PKIA expression through interacting with PKIA promoter. Moreover, SIRT1 silencing compromised dronedarone-mediated suppression of cell hypertrophy, while PKIA upregulation abolished the influences of SIRT1 silencing. More importantly, dronedarone improved TAC surgery-induced MH and impairment of cardiac function of rats via affecting SIRT1/FOXO3/PKIA axis. Conclusions: Dronedarone alleviated MH through mediating SIRT1/FOXO3/PKIA axis, which provide more evidences for dronedarone against MH.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.34 no.5
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• pp.563-569
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• 2001

In order to utilize the processing wastes of squid, chitosan was prepared by intermittent deacetylation treaoent of $\beta-chitin$ contained richly in the pen of squid. Acetylchitosan also was synthesized from squid pen chitosan with anhydrous acetic acid and their characteristics were investigated. The amounts of nitrogen and ash of squid pen chitosan were $5.80.2\% and 0.2\pm0.03\%$ respectively, the yield of squid pen chitosan was $25\pm3\%$, the degree of deacetylation was $92\%$, and the molecular weight was $1.15\times10^6$, Acetyl contents of N-acetylchitosan powder, acetylchitosan bead, N-ACF-1 (N-acetylchitosan film-1) and N-ACF-2 (N-acetylchitosan film-2) were $55.9\%, 63.2\%, 56\% and 58.7\%$ respectively. Two major peaks, amide I ($1,653 cm^{-1}$) and II ($1,558 cm^{-1}$) bent, on FT-IR spectra of the N-acetylchitosan from squid pen were almost similar to these of $\beta-chitin$, While there was a broad single peak at $1,601 cm^{-1}$assigned to be an amide I bend in squid pen chitosan. The CP/MAS NMR spectra of $\beta-chitin$, squid pen chitosan and N-acetylchitosan from squid pen showed a relative broad and single peak at 74 ppm assigned to fifth carbon (C-5) and third carbon (C-3). In case of $\beta-chitin$ and N-acetylchitosan from squid pen, single peak at 74 ppm was showed as the same of $\beta-chitin$ type.

• The Korean Journal of Nuclear Medicine
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• v.38 no.1
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• pp.99-108
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• 2004

Purpose: The ability to noninvasively track the migration of neural progenitor cells would have significant clinical and research implications. We generated stably transfected F3 human neural progenitor cells with human sodium/iodide symporter (hNIS) for noninvasively tracking F3. In this study, the expression patterns of hNIS gene in F3-NIS were examined according to the cultured time and the epigenetic modulation. Materials and Methods: F3 human neural stem cells had been obtained from Dr. Seung U. Kim (Ajou University, Suwon, Korea). hNIS and hygromycin resistance gene were linked with IRES (Internal Ribosome Entry Site) under control of CMV promoter. This construct was transfected to F3 with Liposome. To investigate the restoration of hNIS gene expression in F3-NIS, cells were treated with demethylating agent (5-Azacytidine) and Histone deacetylase inhibitor (Trichostatin A: TSA). The expression of hNIS was measured by I-125 uptake assay and RT-PCR analysis. Results: The iodide uptake of the F3-NIS was higher 12.86 times than F3 cell line. According to the cell passage number, hNIS expression in F3-NIS gradually diminished. After treatment of 5-Azacytidine and TSA with serial doses (up to $20{\mu}M$, up to 62.5nM, respectively) for 24 hours, I-125 uptake and mRNA of hNIS in F3-NIS were increased. Conclusion: These results suggest that hNIS transfected F3 might undergo a change in its biological characters by cell passage. Therefore, the gene ex[ressopm of exogenous gene transferred human stem cell might be affected to the epigenetic modulation such as promoter methylation and Histone deacetylation and to the cell culture conditions.

• Archives of Pharmacal Research
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• v.27 no.4
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• pp.407-414
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• 2004

The expression of CYP3A4 gene is induced by a variety of structurally unrelated xenobiotics including the antibiotic rifampicin, pregnenolone 16-carbonitrile (PCN), and endogenous hormones, that might mediate through steroid and xenobiotic receptor (SXR) system. The molecular mechanisms underlying regulation of CYP3A4 gene expression have not been understood. In order to gain the insight of the molecular mechanism of CYP3A4 gene expression, study has been undertaken to investigate if the histone deacetylation is involved in the regulation of CYP3A4 gene expression by proximal promoter in human hepatoma HepG2 cells. Also we have investigated to see if SXR is involved in the regulation of CYP3A4 proximal promoter activity in human hepatoma HepG2 cells. HepG2 cells were transfected with a plasmid PCYP3A4-Luc containing ${\~}1kb$ of the CYP3A4 proximal promoter region (-863 to +64 bp) in front of a reporter gene, luciferase, in the presence or absence of pSAP-SXR. In HepG2 cells, CYP3A4 inducers, such as rifampicin, PCN and RU486 showed minimal stimulation of CYP3A4 proximal promoter activity in the absence of SXR and histone deacetylase (HDAC) inhibitors. 4-Dimethylamino-H-[4-(2-hydroxycarbamoylvinyl)benzyl]benzamide (IN2001), a new class HDAC inhibitor significantly increased CYP3A4 proximal promoter activity over untreated control cells and rifampicin concomitant treatment with IN2001 increased further CYP3A4 proximal promoter activity that was stimulated by IN2001 The results of this study demon-strated that both HDAC inhibitors and SXR are essential to increase of CYP3A4 proximal promoter activity by CYP3A4 inducers such as PCN, rifampicin, and RU486. Especially SXR seems to be important for the dose dependent response of CYP3A4 inducing chemicals to stimulate CYP3A4 proximal promoter activity. Also this data suggested that HDAC inhibitors seemed to facilitate the CYP3A4 proximal promoter to be activated by chemicals.

• Journal of Korean Society of Environmental Engineers
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• v.22 no.2
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• pp.203-210
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• 2000

The preparative methods of a chitosan-deposited activated carbon and its characteristics were studied by using three kinds of chitosan with different degree of deacetylation and average molecular weight. The procedure was consisted of the dissolution of chitosan into acid solution, impregnation of activated carbon, agitation, evaporation, and drying. When the chitosan-dissolved acid and its concentration, amounts of chitosan deposited, and agitation conditions were changed, the specific surface area, deposition state on surface, and stability were investigated, and amounts of Cr(VI) adsorbed was measured. In the preparation process, it was proper to agitate the chitosan-dissolved acetic acid solution at room temperature for 1hr. In the deposition of chitosan with low molecular weight, the specific surface area of activated carbon was greatly decreased even at low chitosan loading, but in the case of high molecular weight it was not nearly changed to 10wt% loading. It was known that chitosan was uniformly and physically deposited on activated carbon. The chitosan-deposited activated carbon was stable into the solution over about pH 6. The removal of Cr(VI) was remarkably enhanced by adding the adsorption function of chitosan to the surface of activated carbon with about 5wt% chitosan. It may be therefore used as an adsorbent for removing the pollutants in air and wastewater.

• The Korean Journal of Nuclear Medicine
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• v.30 no.3
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• pp.351-360
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• 1996

Chitosan is a polysaccharide of natural orgin obtained by full or partial deacetylation of chitin, a very abudant natural polymer, which has the properties of biocompatibilities, bioaffinities, and biodegradabilities. The free amino group of chitosan should be participated in forming chelate with holmium (${\beta}$-emitter). $^{166}Ho(NO_3)_3\;5H_2O$ of high radionuclidic purity of upto 99.9% was made by neutron irradiation of naturally occuring $^{166}Ho(NO_3)_3\;5H_2O$, and then reacted with the prepared chitosan solution. The effect of pH, reaction time, the concentration and viscosity of chitosan and the amount of $^{166}Ho$ on forming $^{166}Ho$-chitosan complex ($^{166}Ho$-CHICO) were investigated. $^{166}Ho$-chitosan macroaggregate($^{166}Ho$-CHIMA) was made from $^{166}Ho$-CHICO. Their physical properties such as radionuclidic purity, particle size distribution, stability in vitro and vivo were examined. Their high in vitro and vivo stability makes them attractive agents for internal radiotherapy by local administeration.

• Biomolecules & Therapeutics
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• v.25 no.5
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• pp.511-518
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• 2017

Ultraviolet (UV) irradiation is a relevant environment factor to induce cellular senescence and photoaging. Both autophagy- and silent information regulator T1 (SIRT1)-dependent pathways are critical cellular processes of not only maintaining normal cellular functions, but also protecting cellular senescence in skin exposed to UV irradiation. In the present studies, we investigated whether modulation of autophagy induction using a novel synthetic SIRT1 activator, heptasodium hexacarboxymethyl dipeptide-12 (named as Aquatide), suppresses the UVB irradiation-induced skin aging. Treatment with Aquatide directly activates SIRT1 and stimulates autophagy induction in cultured human dermal fibroblasts. Next, we found that Aquatide-mediated activation of SIRT1 increases autophagy induction via deacetylation of forkhead box class O (FOXO) 1. Finally, UVB irradiation-induced cellular senescence measured by $SA-{\beta}-gal$ staining was significantly decreased in cells treated with Aquatide in parallel to occurring SIRT1 activation-dependent autophagy. Together, Aquatide modulates autophagy through SIRT1 activation, contributing to suppression of skin aging caused by UV irradiation.