Liquiritigenin prevents palmitate-induced beta-cell apoptosis via estrogen receptor-mediated AKT activation

Bae, Gong Deuk,Park, Eun-Young,Baek, Dong Jae,Jun, Hee-Sook,Oh, Yoon Sin Elsevier 2018 Biomedicine & pharmacotherapy Vol.101 No.-

<P><B>Abstract</B></P> <P>Liquiritigenin (LQ) is a major active component of licorice root, which is a flavone used for treating many diseases, including diabetes. LQ has been shown to exhibit a glucose-lowering effect in diabetic mice. Therefore, we investigated the potential of LQ to protect against lipotoxicity-induced beta-cell apoptosis and the underlying molecular mechanisms. Exposure of INS-1 rat insulinoma cells to LQ significantly increased cell viability and blocked palmitate (PA)-induced apoptosis, as evidenced by the reduction of Annexin-V-stained cells, cleaved caspase-3 levels, and poly (ADP-ribose) polymerase (PARP) activity, as well as upregulation of Bcl-2 expression. Moreover, LQ treatment significantly reduced the endoplasmic reticulum (ER) stress response by reducing phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK), phosphorylated eIF-2a, and CHOP expression in PA-treated INS-1 cells. The anti-apoptotic effect of LQ treatment was reversed through co-treatment with fulvestrant, a specific inhibitor of the estrogen receptor. LQ also increased AKT phosphorylation, and inactivation of this molecular event failed to decrease PERK phosphorylation with LQ treatment in PA-treated INS-1 cells. This effect was further accompanied by an inability to recover cell viability. These results suggest that LQ protects INS-1 cells from lipotoxicity-induced apoptosis by suppressing ER stress. We conclude that estrogen receptor-mediated AKT phosphorylation is one of the mechanisms contributing to the anti-apoptotic effect of LQ.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Protective effect of liquiritigenin on palmitate induced lipotoxicity in INS-1 cells

Gong deuk Bae,Hee-Sook Jun,Yoon Sin Oh 한국식품영양과학회 2016 한국식품영양과학회 학술대회발표집 Vol.2016 No.10

Phosphorylation of tyrosine-14 on Caveolin-1 enhances lipopolysaccharide-induced inflammation in human intestinal Caco-2 cells

Gong Deuk Bae,Kyong Kim,Se-Eun Jang,Dong-Jae Baek,Eun-Young Park,Yoon Sin Oh 한국응용생명화학회 2023 Journal of Applied Biological Chemistry (J. Appl. Vol.66 No.-

Caveolin-1 (Cav-1) is the main structural component of the caveolae on the plasma membrane, which regulates various cellular processes, including cell growth, differentiation, and endocytosis. Although a recent study demonstrated that Cav-1 might be involved in diabetes-associated inflammation, its exact role in the intestine was unclear. In this study, we examined the intestinal expression of Cav-1 in diabetic conditions. We also investigated its effect on lipopolysaccharide (LPS)-induced inflammation by expressing this protein in human intestinal Caco- 2 cells lacking Cav-1. We observed that increased Cav-1 levels and decreased expression of tight junction proteins affected intestinal permeability in high-fat diet-induced diabetic mice. When Caco-2 cells were treated with LPS, Cav-1 enhanced the NF-κB signaling. Moreover, LPS reduced the expression of tight junction proteins while it increased cell-cell permeability and reactive oxygen species generation in Caco-2 cells and this effect was amplified by cav-1 overexpression. LPS treatment promoted phosphorylation of tyrosine-14 (Y14) on Cav-1, and the LPSinduced NF-κB signaling was suppressed in cells expressing nonphosphorylatable Cav-1 (tyrosine-14 to phenylalanine mutant), which reduced intestinal barrier permeability. These results suggest that Cav-1 expression promotes LPS-induced inflammation in Caco-2 cells, and phosphorylation of Y14 on Cav-1 might contribute to the anti-inflammatory response in LPS-induced NF- κB signaling and cell permeability.

Chromium oxide supported on Zr modified alumina for stable and selective propane dehydrogenation in oxygen free moving bed process

Sim, Seohyun,Gong, Sujin,Bae, Jongyoon,Park, Yong-Ki,Kim, Jongwoo,Choi, Won Choon,Hong, Ung Gi,Park, Deuk Soo,Song, In Kyu,Seo, Hwimin,Kang, Na Young,Park, Sunyoung Elsevier 2017 Molecular catalysis Vol.436 No.-

<P>Propane dehydrogenation in oxygen free environment over alumina-supported chromium oxide catalysts with different chromium loading was studied within short time-on-stream range for the fluidized moving bed applications. For this purpose, a series of CrOx/Al2O3 and CrOxar-Al2O3 catalysts were prepared and examined. Increase in the chromium loading resulted in reduction of monochromate species, possibly leading to formation of polychromate species. Further increase of chromium loading led to formation of Cr2O3 species. Accordingly, specific activity of the catalyst decreased with increasing chromium loading. Propane conversion significantly decreased and propylene selectivity increased during an induction period due to the rapid consumption of limited lattice oxygen in the catalyst. Equilibrated and artificially aged catalysts were characterized in order to investigate the factors affecting propylene selectivity and catalyst durability by pore analysis, temperature-programmed reduction (H-2-TPR), temperature programmed desorption (NH3-TPD), X-ray diffraction patterns (XRD), Raman spectroscopy, and X-ray photoelectron spectroscopy (XPS). After an artificial catalyst aging treatment, all catalysts showed reduction in catalytic activity and the most drastic activity decrease was found in the catalyst with the highest loading of 20 wt% Crhi-Al2O3 sample. The activity loss was mainly due to agglomeration of the chromium species, reduction of the surface area, and transformation of Cr6+ species into stable Cr2O3 species. Cr species were agglomerated on the surface of alumina support during the aging treatment and the agglomeration was more pronounced at the high Cr loading. Moreover, Raman spectroscopy and XRD analyses revealed the formation of chromia/alumina solid solution in the catalyst after the aging treatment which also significantly contributed to the activity loss. Contrarily, Zr modified alumina support successfully suppressed the formation of chromia/alumina solid solution phase and substantially improved the catalytic activity after the aging treatment by increasing the dispersion of chromium oxide. Zr-Al2O3 support showed lower catalytic activity toward propylene than Al2O3 support, which also contributed to the higher propylene yield of Cr/Zr-Al2O3. (C) 2017 Published by Elsevier B.V.</P>

Allomyrina dichotoma larva extract attenuates free fatty acid-induced lipotoxicity in pancreatic beta cells

Kyong Kim,Min-Kyu Kwak,Gong-Deuk Bae,Eun-Young Park,Dong-Jae Baek,Chul-Young Kim,Se-Eun Jang,Hee-Sook Jun,Yoon Sin Oh 한국영양학회 2021 Nutrition Research and Practice Vol.15 No.3

BACKGROUD/OBJECTIVES: Allomyrina dichotoma larva (ADL), one of the many edible insects recognized as future food resources, has a range of pharmacological activities. In a previous study, an ADL extract (ADLE) reduced the hepatic insulin resistance of high-fat diet (HFD)-induced diabetic mice. On the other hand, the associated molecular mechanisms underlying pancreatic beta-cell dysfunction remain unclear. This study examined the effects of ADLE on palmitate-induced lipotoxicity in a beta cell line of a rat origin, INS-1 cells. MATERIALS/METHODS: ADLE was administered to high-fat diet treated mice. The expression of apoptosis-related molecules was measured by Western blotting, and reactive oxidative stress generation and nitric oxide production were measured by DCH-DA fluorescence and a Griess assay, respectively. RESULTS: The administration of ADLE to HFD-induced diabetic mice reduced the hyperplasia, 4-hydroxynonenal levels, and the number of apoptotic cells while improving the insulin levels compared to the HFD group. Treatment of INS-1 cells with palmitate reduced insulin secretion, which was attenuated by the ADLE treatment. Furthermore, the ADLE treatment prevented palmitate-induced cell death in INS-1 cells and isolated islets by reducing the apoptotic signaling molecules, including cleaved caspase-3 and PARP, and the Bax/Bcl2 ratio. ADLE also reduced the levels of reactive oxygen species generation, lipid accumulation, and nitrite production in palmitate-treated INS-1 cells while increasing the ATP levels. This effect corresponded to the decreased expression of inducible nitric oxide synthase (iNOS) mRNA and protein. CONCLUSIONS: ADLE helps prevent lipotoxic beta-cell death in INS-1 cells and HFD-diabetic mice, suggesting that ADLE can be used to prevent or treat beta-cell damage in glucose intolerance during the development of diabetes.

Deep-Level Defects on Nitrogen-Doped ZnO by Photoinduced Current Transient Spectroscopy

Hyun Yul Choi,Dong Hyeok Seo,Dong Wook Kwak,Min Soo Kim,Yu Kyeong Kim,Ho Jae Lee,Dong Hun Song,Jae Hee Kim,Jae Sun Lee,Sung Ho Lee,Deuk Gong Yoon,Jin Sun Bae,Hoon Young Cho 한국진공학회 2013 한국진공학회 학술발표회초록집 Vol.2013 No.2