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Jeong, Gil-Saeng,Lee, Dong-Sung,Li, Bin,Lee, Hwa-Jun,Kim, Eun-Cheol,Kim, Youn-Chul Elsevier 2010 european journal of pharmacology Vol.644 No.1
<P><B>Abstract</B></P><P>Sappanchalcone has been demonstrated to possess several biological effects. However, the molecular mechanism underlying these effects is not fully understood. In this study, we examined the effects of sappanchalcone on hydrogen peroxide (H<SUB>2</SUB>O<SUB>2</SUB>)-induced cytotoxicity using human dental pulp (HDP) cells, and lipopolysaccharide (LPS)-induced inflammation using human periodontal ligament (HPDL) cells. Sappanchalone concentration proportionately increased heme oxygenase (HO)-1 protein expression and enzyme activity in both HDP and HPDL cells. It also protected HDP cells from H<SUB>2</SUB>O<SUB>2</SUB>-induced cytotoxicity and reactive oxygen species production. The cytoprotective effect of sappanchalcone was nullified by HO-1 inhibitor, Tin protoporphyrin (SnPP). Sappanchalcone is seen to inhibit LPS-stimulated nitric oxide (NO), prostaglandin E<SUB>2</SUB> (PGE<SUB>2</SUB>), interlukine-1β (IL-1β), tumor necrosis factor-α (TNF-α), interlukine-6 (IL-6) and interlukine-12 (IL-12) release in addition to inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in HPDL cells. SnPP, a specific inhibitor of HO-1, partly blocked sappanchalcone mediated suppression of inflammatory mediator production, in LPS-stimulated HPDL cells. HDP and HPDL cells treated with sappanchalcone exhibited the transient activation of c-Jun NH2-terminal kinase (JNK) and NF-E2-related factor-2 (Nrf2). The expression of HO-1 protein by sappanchalcone was significantly reduced by pretreatment with JNK inhibitor. In conclusion, induction of HO-1 is an important cytoprotective mechanism by which sappanchalcone protects HDP cells from H<SUB>2</SUB>O<SUB>2</SUB> and in addition it also exhibits anti-inflammatory effects in LPS-stimulated HPDL cells. Thus, sappanchalcone could potentially be a therapeutic approach for periodontal, pulpal and periapical inflammatory lesion.</P>
Effects of Herbal Extracts Used in Oriental Medicines on Heme Oxygenase-1 Expression
Jeong, Gil-Saeng,Oh, Seung-Hwan,Kang, Dae-Gill,Lee, Ho-Sub,Kim, Youn-Chul The Physiological Society of Korean Medicine and T 2006 동의생리병리학회지 Vol.20 No.5
Effects of twenty-three aqueous herbal extracts used in oriental medicines on heme oxygenase (HO)-1 expression were estimated in a mouse hippocampal cell line, HT22. HO-1 is one of the cytoprotective enzymes activated various stimuli, and Western blot analysis was used for evaluated HO-1 expression. Six aqueous extracts such as Rhei Rhizoma, Paeoniae Radix, Uncariae Ramulus et Uncus, Theae Folium, Prunellae Spica, and Coptidis Rhizoma significantly increased HO-1 expression in HT22 cells at the concentration of 300 ${\mu}$g/ml. In Addition, four aqueous extracts including Eucommiae Cortex, Moutan Cortex Radicis, Ginseng Radix Rubra, and Scutellariae Radix moderately increased HO-1 expression. These results would be usefulfor the isolation and identification of their neuroprotective principles.
Jeong, Gil-Saeng,Lee, Dong-Sung,Song, Mi-Young,Park, Byung-Hyun,Kang, Dae-Gill,Lee, Ho-Sub,Kwon, Kang-Beom,Kim, Youn-Chul Pharmaceutical Society of Japan 2011 Biological & pharmaceutical bulletin Vol.34 No.1
<P>Butein (3,4,2′,4′-tetrahydroxychalcone), a plant polyphenol, is a major component in isolate of <I>Rhus verniciflua</I> S<SMALL>TOKES</SMALL> (Anacardiaceae). It is shown to exert various potent effects such as antioxidant, antiinflammatory induction of apoptosis among many properties. In this study, we investigated the effect of butein on cytokine-induced β-cell damage. Pre-treatment with butein is shown to increase the viability of cytokine-treated INS-1 cells at concentrations of 15—30 μ<SMALL>M</SMALL>. Butein prevented cytokine-mediated cell death, as well as nitric oxide (NO) production, and these effects correlated well with reduced levels of protein expression of the inducible nitric oxide synthase (iNOS). Furthermore, the molecular mechanisms by which butein inhibits iNOS gene expression appeared to be through the inhibition of nuclear factor-κB (NF-κB) translocation. In a second set of experiments, rat islets were used to demonstrate the protective effects of butein and the results were essentially the same as those observed in Beutin pretreated INS-1 cells. Butein prevented cytokine-induced NO production, iNOS expression, and NF-κB translocation and inhibition of glucose-stimulated insulin secretion (GSIS). In conclusion, these results suggest that butein can be used for the prevention of functional β-cell damage and preventing the progression of Type 1 diabetes mellitus (T1DM).</P>
Jeong, Gil-Saeng,Li, Bin,Lee, Dong-Sung,Byun, Erisa,An, Ren-Bo,Pae, Hyun-Ock,Chung, Hun-Taeg,Youn, Kwon-Ha,Kim, Youn-Chul Pharmaceutical Society of Japan 2008 Biological & pharmaceutical bulletin Vol.31 No.10
<P>Lavandulyl flavanones of <I>Sophora flavescens</I> roots are anti-malarial, anti-inflammatory, and cytotoxic. Here, we examined whether four lavandulyl flavanones, (2<I>S</I>)-2′-methoxykurarinone (1), sophoraflavanone G (2), leachianone A (3), and (−)-kurarinone (4), isolated from <I>S. flavescens</I> could protect HT22 immortalized hippocampal cells against glutamate-induced oxidative stress. Compounds 1 and 2 induced the expression of heme oxygenase (HO)-1 and increased HO activity dose- and time-dependently. These two compounds also suppressed glutamate-induced reactive oxygen species generation in HT22 cells, whereas compounds 3 and 4 were not protective. These two lavandulyl flavanones (compounds 1, 2) may protect against glutamate-induced neurotoxicity <I>via</I> HO-1 induction.</P>
Jeong, Gil-Saeng,Kwon, Ok-Kyoung,Park, Bo-Young,Oh, Sei-Ryang,Ahn, Kyung-Seop,Chang, Min-Jung,Oh, Won Keun,Kim, Jin-Cheol,Min, Byung-Sun,Kim, Youn-Chul,Lee, Hyeong-Kyu Pharmaceutical Society of Japan 2007 Biological & pharmaceutical bulletin Vol.30 No.7
<P>A new lignan, sylvestrin (1), was isolated from the MeOH-soluble fraction of the roots of <I>Anthriscus sylvestris</I> H<SMALL>OFFM.</SMALL> (Umbelliferae), along with six lignans (2—7), three coumarins (8—10), and a polyacetylene (11). The structure of sylvestrin was determined to be 2-(3′,4′,5′-trimethoxybenzylidene)-3-(3″,4″-methylendioxybenzyl)-γ-butyrolactone (1) by spectroscopic means, including 2D-NMR. The eleven compounds were assessed for their abilities to activate a caspase-3 in human promyeloid leukemic HL-60 cells. The intracellular caspase-3 activity of (−)-deoxypodophyllotoxin (3), angeloyl podophyllotoxin (5), deoxypicropodophyllin (6), picropodophyllotoxin (7), and falcarindiol (11) increased approximately 4.6, 3.6, 3.7, 3.9, and 3.9-fold, at 0.001, 1, 1, 1, and 20 μ<SMALL>M</SMALL>, respectively, over that of the untreated control. In addition, compounds 3, 5, 6, and 7 showed apoptosis-inducing activities that were measured by DNA fragmentation in HL-60 cells.</P>
Jeong, Gil-Saeng,Byun, Erisa,Li, Bin,Lee, Dong-Sung,An, Ren-Bo,Kim, Youn-Chul 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.8
Glutamate-induced oxidative injury causes neuronal degeneration related to many central nervous system diseases, such as Parkinson's disease, Alzheimer's disease, epilepsy and ischemia. The bioassay-guided fractionation of the EtOH extract of the root bark of Dictamnus dasycarpus Trucz. provided one neuroprotective limonoid, obacunone, together with a degraded limonoid, fraxinellone and two alkaloids, dictamine and haplopine. At concentrations of 100-150 ${\mu}M$, obacunone showed the potent neuroprotective effects on glutamate-induced neurotoxicity and induced the expression of heme oxygenase (HO)-1 in the mouse hippocampal HT22 cells. In addition, we found that obacunone increased p38 MAPK phosphorylation and induced HO-1 expression via p38 MAPK pathway. These results suggest that obacunone isolated from the root bark of D. dasycarpus increases cellular resistance to glutamate-induced oxidative injury in mouse hippocampal HT22 cells, presumably through the p38 MAPK pathway-dependent HO-1 expression. These results suggest that obacunone could be the effective candidates for the treatment of ROS-related neurological diseases.
Jeong, Gil-Saeng,Lee, Dong-Sung,Kwon, Tae-Oh,Lee, Hye-Suk,An, Ren-Bo,Kim, Youn-Chul Pharmaceutical Society of Japan 2009 Biological & pharmaceutical bulletin Vol.32 No.5
<P>The bioassay-guided fractionation of a MeOH extract of the heartwood of <I>Caesalpinia sappan</I> L. provided two neuroprotective compounds, sappanchalcone (2) and 4-<I>O</I>-methylepisappanol (3), together with a methoxychalcone, isoliquiritigenin 2′-methyl ether (1), and three aromatic compounds, 4-<I>O</I>-methylsappanol (4), caesalpine J (5), pluchoic acid (6). At concentrations of 20—40 μm, compound 2 showed significant cytoprotective effects against glutamate-induced oxidative stress through the induction of heme oxygenase (HO)-1 in HT22-immortalized hippocampal cells. Compound 3 also showed moderate neuroprotective effect at 40 μm, but compounds 1, 4—6 did not show any protective effects against glutamate-induced cytotoxicity in HT22 cells.</P>