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Kyeong-Rok Kang,Jae-Sung Kim,Jeong-Yeon Seo,HyangI Lim,Tae-Hyeon Kim,Sun-Kyoung Yu,Heung-Joong Kim,Chun Sung Kim,Hong Sung Chun,Joo-Cheol Park,Do Kyung Kim 대한생리학회-대한약리학회 2022 The Korean Journal of Physiology & Pharmacology Vol.26 No.1
The aim of the present study was to investigate the physiological role of nicotinamide phosphoribosyltransferase (NAMPT) associated with odontogenic differentiation during tooth development in mice. Mouse dental papilla cell-23 (MDPC- 23) cells cultured in differentiation media were stimulated with the specific NAMPT inhibitor, FK866, and Visfatin (NAMPT) for up to 10 days. The cells were evaluated after 0, 4, 7, and 10 days. Cell viability was measured using the 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide assay. The mineralization assay was performed by staining MDPC-23 cells with Alizarin Red S solution. After cultivation, MDPC-23 cells were harvested for quantitative PCR or Western blotting. Analysis of variance was performed using StatView 5.0 software (SAS Institute Inc., Cary, NC, USA). Statistical significance was set at p < 0.05. The expression of NAMPT increased during the differentiation of murine odontoblast-like MDPC-23 cells. Furthermore, the up-regulation of NAMPT promoted odontogenic differentiation and accelerated mineralization through an increase in representative odontoblastic biomarkers, such as dentin sialophosphoprotein, dentin matrix protein-1, and alkaline phosphatase in MDPC-23 cells. However, treatment of the cells with the NAMPT inhibitor, FK866, attenuated odontogenic differentiation, as evidenced by the suppression of odontoblastic biomarkers. These data indicate that NAMPT regulated odontoblastic differentiation through the regulation of odontoblastic biomarkers. The increase in NAMPT expression in odontoblasts was closely related to the formation of the extracellular matrix and dentin via the Runx signaling pathway. Therefore, these data suggest that NAMPT is a critical regulator of odontoblast differentiation during tooth development.
Apoptotic activity of demethoxycurcumin in MG-63 human osteosarcoma cells
Kang, Kyeong-Rok,Kim, Jae-Sung,Kim, Tae-Hyeon,Seo, Jeong-Yeon,Park, Jong-Hyun,Chun, Hong Sung,Yu, Sun-Kyoung,Kim, Heung-Joong,Kim, Chun Sung,Kim, Do Kyung The Korean Academy of Oral Biology 2021 International Journal of Oral Biology Vol.46 No.1
Demethoxycurcumin (DMC), which is a curcuminoid found in turmeric, has anti-proliferative effects on cancer cells. However, the effect of DMC on osteosarcoma has not been established. The aim of this study was to examine the effects of DMC on cell growth and apoptosis induction in MG-63 human osteosarcoma cells. This study was investigated using 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromid assay, Live/Dead cell assay, 4', 6-diamidino-2-phenylindole staining, and immunoblotting in MG-63 cells. DMC induced MG-63 cell death in a dose-dependent manner, with an estimated IC50 value of 54.4 µM. DMC treatment resulted in nuclear condensation in MG-63 cells. DMC-induced apoptosis in MG-63 cells was mediated by the expression of Fas and activation of caspase-8, caspase-3, and poly (ADP-ribose) polymerase. Immunoblotting results showed that Bcl-2 and Bcl-xL were downregulated, while Bax and Bad were upregulated by DMC in MG-63 cells. These results indicated that DMC inhibits cell proliferation and induces apoptotic cell death in MG-63 human osteosarcoma cells via the death receptor-mediated extrinsic apoptotic pathway and mitochondria-mediated intrinsic apoptotic pathway.
Kyeong-Rok Kang,Jae-Sung Kim,Tae-Hyeon Kim,Jeong-Yeon Seo,Jong-Hyun Park,Jin Woong Lim,Sun-Kyoung Yu,Heung-Joong Kim,Sang Hun Shin,Bo-Ram Park,Chun Sung Kim,Do Kyung Kim 대한구강생물학회 2020 International Journal of Oral Biology Vol.45 No.3
Acacetin, which is present in damiana (Turnera diffusa ) and black locust (Robinia pseudoacacia ), has several pharmacologic activities such as antioxidant, anti-inflammatory, and anti-proliferative effects on cancer cells. However, the effect of acacetin on head and neck cancers has not been clearly established. This study aimed to examine the effects of acacetin on cell growth and apoptosis induction in FaDu human pharyngeal carcinoma cells. These were investigated by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay, Live/Dead cell assay, 4′,6-diamidino-2-phenylindole dihydrochloride staining, caspase-3 and caspase-7 activation assay, and immunoblotting in FaDu cells. Acacetin induced FaDu cell death in a dose-dependent manner, with an estimated IC50 value of 41.9 µM, without affecting the viability of L-929 mouse fibroblasts as normal cells. Acacetin treatment resulted in nuclear condensation in the FaDu cells. It promoted the proteolytic cleavage of procaspase-3, -7, -8, and -9 with increasing amounts of the cleaved caspase isoforms in FaDu cells. Acacetin-induced apoptosis in FaDu cells was mediated by the expression of Fas and activation of caspase-8, caspase-3, and poly (ADP-ribose) polymerase. Immunoblotting showed downregulation of the anti-apoptotic mitochondrial proteins Bcl-2 and Bcl-xL, but upregulation of the mitochondria-dependent pro-apoptotic proteins Bax and Badin FaDu cells after acacetin treatment. These findings indicate that acacetin inhibits cell proliferation and induces apoptotic cell death in FaDu human pharyngeal carcinoma cells via both the death receptor-mediated extrinsic apoptotic pathway and the mitochondria-mediated intrinsic apoptotic pathway.
Arctigenin induces caspase-dependent apoptosis in FaDu human pharyngeal carcinoma cells
Kang Kyeong-Rok,Kim Jae-Sung,Lim HyangI,Seo Jeong-Yeon,Park Jong-Hyun,Chun Hong Sung,Yu Sun-Kyoung,Kim Heung-Joong,Kim Chun Sung,김도경 대한약리학회 2022 The Korean Journal of Physiology & Pharmacology Vol.26 No.6
The present study was carried out to investigate the effect of Arctigenin on cell growth and the mechanism of cell death elicited by Arctigenin were examined in FaDu human pharyngeal carcinoma cells. To determine the apoptotic activity of Arctigenin in FaDu human pharyngeal carcinoma cells, cell viability assay, DAPI staining, caspase activation analysis, and immunoblotting were performed. Arctigenin inhibited the growth of cells in a dose-dependent manner and induced nuclear condensation and fragmentation. Arctigenin-treated cells showed caspase-3/7 activation and increased apoptosis versus control cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was up-regulated by Arctigenin treatment. Moreover, caspase-8, a part of the extrinsic apoptotic pathway, was activated by Arctigenin treatments. Expressions of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondria-dependent intrinsic apoptosis pathway, significantly decreased following Arctigenin treatment. The expressions of pro-apoptotic factors such as BAX, BAD and caspase-9, and tumor suppressor -53 increased by Arctigenin treatments. In addition, Arctigenin activated caspase-3 and poly (ADP-ribose) polymerase (PARP) induced cell death. Arctigenin also inhibited the proliferation of FaDu cells by the suppression of p38, NF-κB, and Akt signaling pathways. These results suggest that Arctigenin may inhibit cell proliferation and induce apoptotic cell death in FaDu human pharyngeal carcinoma cells through both the mitochondria-mediated intrinsic pathway and the death receptormediated extrinsic pathway. INTRODUCTION Head and neck cancers such as oral cancer, pharyngeal cancer, and laryngeal cancer are the most common cancers worldwide, especially in South America, Asia, and Europe [1-3]. Also, most of them are squamous cell carcinoma [4]. In the last 30 years, the survival rate of head and neck cancer has not improved significantly despite modern medical techniques and treatments such as the use of anticancer drugs [3,5]. Clinical treatment for head and neck cancer may induce adverse effects related to functional changes
Apoptotic effects of hyperoside on FaDu human pharyngeal carcinoma cells
( Kyeong-rok Kang ),( Jeong-yeon Seo ),( Hyangi Lim ),( Jae-sung Kim ),( Do Kyung Kim ) 조선대학교 치의학연구원 2023 Oral Biology Research (Oral Biol Res) Vol.47 No.4
Hyperoside (quercetin 3-o-β-d-galactopyranoside) is a flavonoid glycoside with antidepressant, anti-inflammatory, and anti-cancer effects. However, it is not known whether it is effective for oral cancer. This study aimed to investigate the effects of hyperoside on induction of apoptosis in FaDu human pharyngeal carcinoma cells. It employed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, live/dead staining, 4′,6-diamidino-2-phenylindole (DAPI) staining, hematoxylin and eosin staining, and western blotting to analyze FaDu cells. The MTT assay, live/dead staining, and DAPI staining showed that hyperoside increased FaDu cell apoptosis in a concentration-dependent manner. Hyperoside-induced apoptosis in FaDu cells was mediated by the expression of Fas and activation of caspase-8, caspase-3, and poly (ADP-ribose) polymerase. Western blotting results showed that Bcl-2 and Bcl-xL were downregulated but Bad and Bax were upregulated by hyperoside in FaDu cells. These results suggest that hyperoside inhibits cell proliferation in FaDu human pharyngeal carcinoma cells and induces apoptosis through receptor-mediated extrinsic apoptosis and mitochondrial-mediated endogenous apoptosis pathways.
Synthesis and Characterization of β-Tricalcium Phosphate Derived From Haliotis sp. Shells :
Kang, Kyeong-Rok,Piao, Zheng-Gang,Kim, Jae-Sung,Cho, In-A,Yim, Min-Ji,Kim, Bok-Hee,Oh, Ji-Su,Son, Jun Sik,Kim, Chun Sung,Kim, Do Kyung,Lee, Sook-Young,Kim, Su-Gwan Ovid Technologies (Wolters Kluwer) - Lippincott Wi 2017 Implant dentistry Vol.26 No.3
<P>Conclusions: beta-TCP (Ca-3(PO4)(2)) synthesized from abalone shell can be used as a potential source of bone grafting material.</P>
Kang, Kyeong-Rok,Kim, Jae-Sung,Kim, Tae-Hyeon,Seo, Jeong-Yeon,Lim, HyangI,Park, Jong-Hyun,Yang, Kwang Yeol,Yu, Sun-Kyoung,Kim, Heung-Joong,Kim, Chun Sung,Chun, Hong Sung,Lee, Dong-Seol,Park, Joo-Cheol The Korean Academy of Oral Biology 2021 International Journal of Oral Biology Vol.46 No.1
Alpha-lipoic acid (ALA) is a naturally occurring antioxidant and has been previously used to treat diabetes and cardiovascular disease. However, the autophagy effects of ALA against oxidative stress-induced dopaminergic neuronal cell injury remain unclear. The aim of this study was to investigate the role of ALA in autophagy and apoptosis against oxidative stress in the SH-SY5Y human dopaminergic neuronal cell line. We examined SH-SY5Y phenotypes using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay (cell viability/proliferation), 4′,6-diamidino-2-phenylindole dihydrochloride nuclear staining, Live/Dead cell assay, cellular reactive oxygen species (ROS) assay, immunoblotting, and immunocytochemistry. Our data showed ALA attenuated hydrogen peroxide (H2O2)-induced ROS generation and cell death. ALA effectively suppressed Bax up-regulation and Bcl-2 and Bcl-xL down-regulation. Furthermore, ALA increased the expression of the antioxidant enzyme, heme oxygenase-1. Moreover, the expression of Beclin-1 and LC-3 autophagy biomarkers was decreased by ALA in our cell model. Combined, these data suggest ALA protects human dopaminergic neuronal cells against H2O2-induced cell injury by inhibiting autophagy and apoptosis.
Kim, Kyeong-Rok,Kang, Jun,Chae, Kyu-Jung Pergamon Press 2017 International journal of hydrogen energy Vol.42 No.45
<P><B>Abstract</B></P> <P>Electromethanogenesis is a form of electrobiofuel production through a microbial electrolysis cell (MEC) where methane (CH<SUB>4</SUB>) is directly produced from an electrical current and carbon dioxide (CO<SUB>2</SUB>) using a cathode. With the aim of maximizing methanogenesis in an MEC, this study utilized granular activated carbon (GAC) and a transition metal catalyst to fabricate nickel (Ni) nanoparticle (NP)-loaded GAC (NiNP/GAC) composites and incorporated these into MECs. In this set-up, GAC acted as the main electrical conduit for direct interspecies electron transfer (DIET) between exoelectrogens and methanogenic electrotrophs, and the Ni NPs served as a catalyst to further improve microbe-to-GAC electron transfer. The NiNP/GAC-composites were prepared using two different methods (microwave irradiation and solution plasma ionization). The Ni NPs were determined to be well doped on the GAC surface according to a field emission scanning electron microscope (FE-SEM) and energy-dispersive X-ray (EDX) spectroscopy analysis. Adding GAC into MECs improved CH<SUB>4</SUB> production. The NiNP/GAC composites prepared by solution plasma ionization showed the highest CH<SUB>4</SUB> production (20.7 ml), followed by the NiNP/GAC composite prepared by microwave irradiation (19.6 ml), bare GAC (15.6 ml), and GAC-free control (9.6 ml). In the methanogenic MECs, 40.6% of CH<SUB>4</SUB> was produced from an electrode reaction (i.e., reduction of CO<SUB>2</SUB> to CH<SUB>4</SUB>), and the remaining 59.4% was generated by nonelectrode reactions.</P> <P><B>Highlights</B></P> <P> <UL> <LI> To maximize electromethanogenesis, Ni nanoparticles were doped on granular activated carbon (GAC). </LI> <LI> Ni nanoparticle-loaded GAC composites (NiNP/GAC) were synthesized and incorporated into MECs. </LI> <LI> NiNP/GAC-composites were prepared by the microwave irritation and solution plasma method. </LI> <LI> Incorporating NiNP/GAC-composites into MECs improved the methane production. </LI> <LI> In the methanogenic-MECs, 40.6% of methane was produced from the electrode reaction. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>