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HongRan Choi,
WonBong Lim, InAe Kim,
JiSun Kim,
YoungJong Ko,
HyukIl Kwon,
SangWoo Kim,
K. M. Ahsan Kabir,
Xiaojie Li,
Oksu Kim,
YoungJoon Lee,
SeoYune Kim,
OkJoon Kim
[show abstract]
[hide abstract]
ABSTRACT: Human gingival fibroblasts (hGFs) play an important role in the inflammatory reaction to lipopolysaccharide (LPS) from P. gingivalis, which infects periodontal connective tissue. In addition, although light-emitting diode (LED) irradiation has been reported
to have biostimulatory effects, including anti-inflammatory activity, the pathological mechanisms of these effects are unclear.
This study examined the effects of 635-nm irradiation of P. gingivalis LPS-treated human gingival fibroblasts on inflammatory cytokine profiles and the mitogen-activated protein kinase (MAPK)
pathway, which is involved in cytokine production. Gingival fibroblasts treated or not treated with P. gingivalis LPS were irradiated with 635-nm LED light, and cytokine profiles in the supernatant were assessed using a human inflammation
antibody array. Expression of cyclooxyginase-2 (COX-2) protein and phosphorylation of extracellular signal-regulated kinase
(ERK 1/2), p38, and c-Jun-N-terminal kinase (JNK) were assessed by Western-blot analysis to determine the effects on the MAPK
pathway, and prostaglandin E2 (PGE2) in the supernatant was measured using an enzyme-linked immunoassay. COX-2 protein expression and PGE2 production were significantly increased in the LPS-treated group and decreased by LED irradiation. LPS treatment of gingival
fibroblasts led to the increased release of the pro-inflammatory-related cytokines interleukin-6 (IL-6) and IL-8, whereas
LED irradiation inhibited their release. Analysis of MAPK signal transduction revealed a considerable decrease in p38 phosphorylation
in response to 635-nm radiation either in the presence or absence of LPS. In addition, 635-nm LED irradiation significantly
promoted JNK phosphorylation in the presence of LPS. LED irradiation can inhibit activation of pro-inflammatory cytokines,
mediate the MAPK signaling pathway, and may be clinically useful as an anti-inflammatory tool.
KeywordsLight emitting diode irradiation–Inflammation–Cytokine–PGE2
Lasers in Medical Science 05/2012; 27(2):459-467. · 2.00 Impact Factor
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HongRan Choi,
WonBong Lim, InAe Kim,
JiSun Kim,
YoungJong Ko,
Hyukil Kwon,
SangWoo Kim,
K M Ahsan Kabir,
Xiaojie Li,
Oksu Kim,
YoungJoon Lee,
SeoYune Kim,
OkJoon Kim
[show abstract]
[hide abstract]
ABSTRACT: Human gingival fibroblasts (hGFs) play an important role in the inflammatory reaction to lipopolysaccharide (LPS) from P. gingivalis, which infects periodontal connective tissue. In addition, although light-emitting diode (LED) irradiation has been reported to have biostimulatory effects, including anti-inflammatory activity, the pathological mechanisms of these effects are unclear. This study examined the effects of 635-nm irradiation of P. gingivalis LPS-treated human gingival fibroblasts on inflammatory cytokine profiles and the mitogen-activated protein kinase (MAPK) pathway, which is involved in cytokine production. Gingival fibroblasts treated or not treated with P. gingivalis LPS were irradiated with 635-nm LED light, and cytokine profiles in the supernatant were assessed using a human inflammation antibody array. Expression of cyclooxyginase-2 (COX-2) protein and phosphorylation of extracellular signal-regulated kinase (ERK 1/2), p38, and c-Jun-N-terminal kinase (JNK) were assessed by Western-blot analysis to determine the effects on the MAPK pathway, and prostaglandin E(2) (PGE(2)) in the supernatant was measured using an enzyme-linked immunoassay. COX-2 protein expression and PGE(2) production were significantly increased in the LPS-treated group and decreased by LED irradiation. LPS treatment of gingival fibroblasts led to the increased release of the pro-inflammatory-related cytokines interleukin-6 (IL-6) and IL-8, whereas LED irradiation inhibited their release. Analysis of MAPK signal transduction revealed a considerable decrease in p38 phosphorylation in response to 635-nm radiation either in the presence or absence of LPS. In addition, 635-nm LED irradiation significantly promoted JNK phosphorylation in the presence of LPS. LED irradiation can inhibit activation of pro-inflammatory cytokines, mediate the MAPK signaling pathway, and may be clinically useful as an anti-inflammatory tool.
Lasers in Medical Science 08/2011; 27(2):459-67. · 2.00 Impact Factor
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WonBong Lim,
OkSu Kim,
JinAn Jung,
YoungJong Ko,
JooWon Ha,
HeeKyun Oh,
HoiSoon Lim,
Hyukil Kwon, InAe Kim,
Jisun Kim,
MiSook Kim,
SeoYune Kim,
Byung-kuk Kim,
SunMi Kim,
Byung-Cheol Kang,
HongRan Choi,
OkJoon Kim
[show abstract]
[hide abstract]
ABSTRACT: A growing body of evidence shows that compounds of plant origin have the ability to prevent cancer. The fruit of gardenia, Gardenia jasminoides Ellis (Rubiaceae), has long been used as a food additive and herbal medicine, and its pharmacological actions, such as protective activity against oxidative damage, cytotoxic effect, and anti-inflammatory and anti-tumor activity, have already been reported.
The purpose of the present study was to investigate the presence of DNA topoisomerase 1 inhibitor in various solvent fractions of Gardenia extract and examine the induction of oral cancer cell death upon treatment with Gardenia extract.
The methanol extract of Gardenia was partitioned with n-hexane, dichloromethane, ethyl acetate, n-butanol, and water.
In the DNA topoisomerase 1 assay, n-hexane and dichloromethane fractions inhibited topoisomerase 1 and led to a decrease in the cell viability of KB cells. The dichloromethane fraction (0.1 mg/mL) also showed 77% inhibition of cell viability in KB cells compared with HaCaT cells. Treatment with dichloromethane fraction led to apoptotic cell death as evidenced by flow cytometric analysis and morphological changes. In addition, treatment with Gardenia extract dichloromethane fraction led to the partial increase of caspase-3, caspase-8 and caspase-9 activities and the cleavage of poly (ADP-ribose) polymerase.
Taken together, these results suggest that the dichloromethane fraction from Gardenia extract induces apoptotic cell death by DNA topoisomerase 1 inhibition in KB cells. These findings suggest the possibility that Gardenia extract could be developed as an anticancer modality.
Pharmaceutical Biology 12/2010; 48(12):1354-60. · 0.88 Impact Factor
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HyukIl Kwon,
WonBong Lim,
YooDuk Choi,
JongHee Nam,
ChangWoo Han,
JiSun Kim,
YoungJong Ko, InAe Kim,
SeoYune Kim,
MiSook Kim,
OkSu Kim,
HongRan Choi,
OkJoon Kim
[show abstract]
[hide abstract]
ABSTRACT: An oncocytic mucoepidermoid carcinoma arising from the minor salivary gland origin is extremely rare. We report on a 44-year-old man with a high-grade oncocytic mucoepidermoid carcinoma originating in the minor salivary gland of the posterior mandible. All tumor cells showed the expected pattern of immunoreactivity, with positive results for the antimitochondrial antibody and p63, and negative results for the androgenic receptor antibody. Microscopically, the tumor was considered to be a high-grade carcinoma in the grading systems of the Armed Forces Institute of Pathology and Brandwein. The patient underwent a partial mandibulectomy, and the lesion was reconstructed with a right fibula osteofasciocutaneous flap under general anesthesia. The patient is currently under long-term follow-up.
Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics 06/2010; 109(6):e72-7. · 1.50 Impact Factor
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[show abstract]
[hide abstract]
ABSTRACT: Poor interaction between cells and surfaces, especially hydrophobic surfaces, results in delayed proliferation and increased apoptosis due to low cell adhesion signaling. To improve cell adhesion, hydrophilic array of amorphous calcium phosphate (ACP) was fabricated on a surface. A phosphate-buffered solution containing calcium ions was prepared at low temperature to prevent spontaneous precipitation. Then, the ion solution was heated to generate nuclei of ACP nanoparticles. The ACP nanoparticles adhered to the hydrophobic polystyrene surface forming an array composed of ACP particles. Multiple treatments of these nuclei with fresh CaP ion solutions increased the diameter and decreased the solubility of ACP particles enough to mediate cellular adhesion. The particle density in the array was dependent on the ion concentration of the CaP ion solutions. The ACP array improved a wide variety of activities when osteoblastic MC3T3-E1 cells were cultured on the ACP array fabricated on a hydrophobic bacteriological dish surface, compared to those cultured without the ACP array in vitro. The use of ACP array resulted in a lower apoptosis and also increased the spreading of cells to form stress fibers and focal contacts. Cells cultured on the ACP array proliferated more than cells cultured on a hydrophobic surface without the ACP array. The ACP array increased the expression of markers of differentiation in osteoblast. These results indicate that an array of ACP can be used as a coating material for enhancing biocompatibility in tissue engineering or biomaterials rather than modifying the surface with organic molecules.
Journal of Biomedical Materials Research Part B Applied Biomaterials 04/2010; 93(1):113-21. · 2.15 Impact Factor
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WonBong Lim,
Jae-Hyung Kim,
EunByul Gook,
JiSun Kim,
YoungJong Ko, InAe Kim,
Hyukll Kwon,
HoiSoon Lim,
ByungCho Jung,
KyuHo Yang,
NamKi Choi,
MiSook Kim,
SeoYune Kim,
HongRan Choi,
OkJoon Kim
[show abstract]
[hide abstract]
ABSTRACT: Nitric oxide (NO) is a major factor contributing to the loss of neurons in ischemic stroke, demyelinating diseases, and other neurodegenerative disorders. NO not only functions as a direct neurotoxin, but also combines with superoxide (O(2)(-)) by a diffusion-controlled reaction to form peroxynitrite (ONOO(-)), a species that contributes to oxidative signaling and cellular apoptosis. However, the mechanism by which ONOO(-) induces apoptosis remains unclear, although subsequent formation of reactive oxygen species (ROS) has been suggested. The aim of this study was to further investigate the triggers of the apoptotic pathway using O(2)(-) scavenging with light irradiation to block ONOO(-) production. Antiapoptotic effects of light irradiation in sodium nitroprusside (SNP)-treated SH-SY5Y cells were assayed by reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, DNA fragmentation, flow cytometry, Western blot, and caspase activity assays. In addition, NO, total ROS, O(2)(-), and ONOO(-) levels were measured to observe changes in NO and its possible involvement in radical induction. Cell survival was reduced to approximately 40% of control levels by SNP treatment, and this reduction was increased to 60% by low-level light irradiation. Apoptotic cells were observed in the SNP-treated group, but the frequency of these was reduced in the irradiation group. NO, O(2)(-), total ROS, and ONOO(-) levels were increased after SNP treatment, but O(2)(-), total ROS, and ONOO(-) levels were decreased after irradiation, despite the high NO concentration induced by SNP treatment. Cytochrome c was released from mitochondria of SNP-treated SH-SY5Y cells, but not of irradiated cells, resulting in a decrease in caspase-3 and -9 activity in SNP-treated cells. Finally, these results show that 635-nm irradiation, by promoting the scavenging of O(2)(-), protected against neuronal death through blocking the mitochondrial apoptotic pathway induced by ONOO(-) synthesis.
Free radical biology & medicine 07/2009; 47(6):850-7. · 5.42 Impact Factor
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Hongran Choi,
Wonbong Lim,
Ji-Eun Kim, Inae Kim,
Jinan Jeong,
Youngjong Ko,
Jongwoon Song,
Sunyeol You,
Doman Kim,
Misook Kim,
Byung-Kuk Kim,
Okjoon Kim
[show abstract]
[hide abstract]
ABSTRACT: The objective of this study is to investigate the effect of intracellular photosensitizer distribution on tumor cell death after photodynamic therapy (PDT).
The photosensitizer accumulates in tumor tissue during PDT, and generates intracellular reactive oxygen species (ROS), resulting in tumor cell death.
This study was carried out to elucidate the effects of PDT in a KB oral cancer cell line using hematoporphyrin with irradiation at 635 nm and 5 mW/cm(2). After irradiation, the MTT reduction method, agarose gel electrophoresis, flow cytometry, and Diff-Quick staining were performed. The intracellular ROS level was measured by DCF-DA. Intracellular hematoporphyrin was monitored with a confocal microscope, and Western blot and caspase activity assays were performed.
In our study, cell survival was reduced by about 50% after 3 h of hematoporphyrin incubation time. In DNA fragmentation, flow cytometry, and Diff-Quick assay, necrosis was identified within 12 h and apoptosis soon thereafter. Confocal microscopy revealed that hematoporphyrin was localized in the cell membrane, cytoplasm, and nucleus as time passed. The quantities of intracellular ROS correlated with the time of hematoporphyrin accumulation. Additionally, Western blot analysis of Bcl-2/Bax, the release of cytochrome C, and activity of caspase-3 and caspase-9 showed that apoptosis followed the mitochondria-dependent pathway.
PDT with hematoporphyrin in the KB cell line showed morphological changes of cell necrosis and apoptosis, which were associated with the time of distribution and localization of hematoporphyrin. Also, the apoptosis evoked followed the mitochondria-dependent pathway.
Photomedicine and laser surgery 06/2009; 27(3):453-60. · 1.76 Impact Factor
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Wonbong Lim,
Mikyung Ko,
Sungga Lee, Inae Kim,
Mina Jung,
Okjoon Kim,
Seonghoun Cho,
Kyuho Yang,
Namki Choi,
Sunmi Kim,
Hongran Choi
[show abstract]
[hide abstract]
ABSTRACT: The purpose of this study was to examine the protection afforded by 635-nm irradiation against ultraviolet (UV)-C-induced apoptosis in primary human gingival fibroblasts (hGFs).
UV irradiation is known to cause photoaging and cellular apoptosis of skin cells and is considered to be one of the leading causes of skin carcinogenesis.
To induce apoptosis, UV-C (100 mJ/cm2) was used to irradiate hGFs. To protect them from apoptosis, pretreatment with 635-nm irradiation was performed for 1 h immediately after cell plating 36 or 48 h before UV-C irradiation. The light source used for irradiation was a continuous-wave 635-nm LED laser emitting at 1 mW/cm2. Experimental samples were selected 24 h after UV-C irradiation. To measure the numbers of apoptotic cells, MTT assay and flow cytometric analyses were performed. For histomorphologic findings, Diff-Quick staining was carried out. Also, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were measured.
In the present study, the number of apoptotic cells declined in the cells that were pretreated with 635-nm light irradiation in a time-dependent manner. In addition, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were significantly recovered by pretreatment with 635-nm irradiation.
These results suggest that 635-nm visible light irradiation may be used as a protective tool to prevent UV-C-induced apoptosis.
Photomedicine and Laser Surgery 07/2008; 26(3):215-20. · 1.25 Impact Factor
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[show abstract]
[hide abstract]
ABSTRACT: Inhibition of cyclooxygenase (COX) and prostaglandin E(2) (PGE(2)) protects cells against cell injury in specific pathophysiological situations: inflammation and oxidative stress. Although the anti-inflammatory effects have been reported in clinical fields for specific wavelength irradiation during wound healing, the physiological mechanism has not been clarified yet. The aim of the present study is to investigate the anti-inflammatory mechanism of 635 nm light-emitting-diode (LED) irradiation compared with existing COX inhibitors.
The present study investigated anti-inflammatory effects of 635 nm irradiation on PGE(2) release, COX and phospholipase A(2) (PLA(2)) expression, and reactive oxygen species (ROS) dissociation in arachidonic acid (AA)-treated human gingival fibroblast (hGF). These results were compared with their existing COX inhibitors: indomethacin and ibuprofen. The PGE(2) release was measured by enzyme immunoassay, the COX expression was measured by western blot and reverse transcriptase polymerase chain reaction (RT-PCR), and ROS level was measured by flow cytometry, laser scanning confocal microscope and RT-PCR.
Results showed that 635 nm irradiation and existing COX inhibitors inhibit expression of COX and PGE(2) release. Unlike indomethacin and ibuprofen, 635 nm irradiation leads to a decrease of ROS levels and mRNA expression of cytosolic phospholipase A(2) (cPLA(2)) and secretary phospholipase A(2) (sPLA(2)).
Taken together, 635 nm irradiation, unlike indomethacin and ibuprofen, can directly dissociate the ROS. This inhibits cPLA(2), sPLA(2), and COX expression, and results in the inhibition of PGE(2) release. Thus, we suggest that 635 nm irradiation inhibits PGE(2) synthesis like COX inhibitor and appears to be useful as an anti-inflammatory tool.
Lasers in Surgery and Medicine 09/2007; 39(7):614-21. · 2.75 Impact Factor
