Hee-Chul Ko
Jeju National University
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Publication
Featured researches published by Hee-Chul Ko.
Biochemical and Biophysical Research Communications | 2011
Seong-Il Kang; Hee-Chul Ko; Hye-Sun Shin; Hyo-Min Kim; Youn-Suk Hong; Nam-Ho Lee; Se-Jae Kim
Progression of 3T3-L1 preadipocyte differentiation is divided into early (days 0-2, D0-D2), intermediate (days 2-4, D2-D4), and late stages (day 4 onwards, D4-). In this study, we investigated the effects of fucoxanthin, isolated from the edible brown seaweed Petalonia binghamiae, on adipogenesis during the three differentiation stages of 3T3-L1 preadipocytes. When fucoxanthin was applied during the early stage of differentiation (D0-D2), it promoted 3T3-L1 adipocyte differentiation, as evidenced by increased triglyceride accumulation. At the molecular level, fucoxanthin increased protein expression of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), sterol regulatory element-binding protein 1c (SREBP1c), and aP2, and adiponectin mRNA expression, in a dose-dependent manner. However, it reduced the expression of PPARγ, C/EBPα, and SREBP1c during the intermediate (D2-D4) and late stages (D4-D7) of differentiation. It also inhibited the uptake of glucose in mature 3T3-L1 adipocytes by reducing the phosphorylation of insulin receptor substrate 1 (IRS-1). These results suggest that fucoxanthin exerts differing effects on 3T3-L1 cells of different differentiation stages and inhibits glucose uptake in mature adipocytes.
Biochemical and Biophysical Research Communications | 2013
Seon-A Yoon; Seong-Il Kang; Hye-Sun Shin; Seung-Woo Kang; Jeong-Hwan Kim; Hee-Chul Ko; Se-Jae Kim
p-Coumaric acid (3-[4-hydroxyphenyl]-2-propenoic acid) is a ubiquitous plant metabolite with antioxidant, anti-inflammatory, and anticancer properties. In this study, we examined whether p-coumaric acid modulates glucose and lipid metabolism via AMP-activated protein kinase (AMPK) in L6 skeletal muscle cells. p-Coumaric acid increased the phosphorylation of AMPK in a dose-dependent manner in differentiated L6 skeletal muscle cells. It also increased the phosphorylation of acetyl-CoA carboxylase (ACC) and the expression of CPT-1 mRNA and PPARα, suggesting that it promotes the β-oxidation of fatty acids. Also, it suppressed oleic acid-induced triglyceride accumulation, and enhanced 2-NBDG uptake in differentiated L6 muscle cells. Pretreatment with compound C inhibited AMPK activation, reduced ACC phosphorylation and 2-NBDG uptake, and increased triglyceride accumulation. However, p-coumaric acid counterbalanced the inhibitory effects of compound C. Taken together, these results suggest that p-coumaric acid modulates glucose and lipid metabolism via AMPK activation in L6 skeletal muscle cells and that it has potentially beneficial effects in improving or treating metabolic disorders.
Journal of Agricultural and Food Chemistry | 2012
Seong-Il Kang; Hye-Sun Shin; Hyo-Min Kim; Seon-A Yoon; Seung-Woo Kang; Jeong-Hwan Kim; Hee-Chul Ko; Se-Jae Kim
In this study, we investigated the antiobesity properties of Petalonia binghamiae extract (PBE) in mice in which obesity was induced with a high-fat diet (HFD). PBE administration (150 mg/kg/day) for 70 days decreased body weight gain, adipose tissue weight, and the serum triglyceride level in mice fed a HFD. PBE reduced serum levels of glutamic pyruvic transaminase and glutamic oxaloacetic transaminase as well as the accumulation of lipid droplets in the liver. PBE restored the HFD-induced decrease in phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) in epididymal adipose tissue. PBE increased the phosphorylation of AMPK and ACC and decreased the expression of SREBP1c in mature 3T3-L1 adipocytes. In addition, we further explored the active compound responsible for AMPK activation by PBE in 3T3-L1 adipocytes. Fucoxanthin isolated from PBE increased the phosphorylation of AMPK and ACC with increasing LKB1 phosphorylation in mature 3T3-L1 adipocytes. Taken together, these data suggest that PBE (or fucoxanthin) exert improving effects on HFD-induced obesity by promoting β-oxidation and reducing lipogenesis.
Journal of Nutritional Biochemistry | 2010
Seong-Il Kang; Moo-Han Kim; Hye-Sun Shin; Hyo-Min Kim; Youn-Suk Hong; Ji-Gweon Park; Hee-Chul Ko; Nam-Ho Lee; Wan-Seok Chung; Se-Jae Kim
We previously showed that an ethanolic extract of the edible brown algae Petalonia binghamiae promotes the differentiation of 3T3-L1 preadipocytes and decreases hyperglycemia in streptozotocin-induced diabetic mice. Here, we report that a water-soluble extract of P. binghamiae thalli, prepared by enzymatic digestion, inhibits preadipocyte differentiation and adipogenesis in a dose-dependent manner. In differentiating 3T3-L1 preadipocytes, the extract (designated PBEE) decreased the expression of peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding proteins α and β, and fatty acid-binding protein aP2. It also inhibited the mitotic clonal expansion process of adipocyte differentiation, and it inhibited insulin-stimulated uptake of glucose into mature 3T3-L1 adipocytes by reducing phosphorylation of insulin receptor substrate-1. In rats with high-fat diet (HFD)-induced obesity, PBEE exhibited potent anti-obesity effects. In this animal model, increases in body weight and fat storage were suppressed by the addition of PBEE to the drinking water at 500 mg/L for 30 days. PBEE supplementation reduced serum levels of glutamic pyruvic and glutamic oxaloacetic transaminases and increased the serum level of high-density lipoprotein cholesterol. Moreover, it significantly decreased the accumulation of lipid droplets in liver tissue, suggesting a protective effect against HFD-induced hepatic steatosis. Taken together, these data demonstrate that PBEE inhibits preadipocyte differentiation and adipogenesis in cultured cells and in rodent models of obesity.
Food and Chemical Toxicology | 2013
Seung-Woo Kang; Seong-Il Kang; Hye-Sun Shin; Seon-A Yoon; Jeong-Hwan Kim; Hee-Chul Ko; Se-Jae Kim
In this study, we investigated the effects of Sasa quelpaertensis Nakai extract (SQE) and its main constituent, p-coumaric acid, on adipogenesis in 3T3-L1 cells. SQE markedly inhibited adipogenesis by downregulating the expression of CCAAT/enhancer-binding protein α (C/EBPα), peroxisome proliferator-activated receptor γ (PPARγ), sterol regulatory element-binding protein-1c (SREBP-1c), and aP2. It also decreased the expression of fatty acid synthase (FAS) and adiponectin mRNAs in differentiating adipocytes. SQE increased AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) phosphorylation during the early phase of MDI-induced differentiation, suggesting that SQE exerted its anti-adipogenic effect via AMPK activation at an early stage of the differentiation process. p-Coumaric acid suppressed adipogenesis by attenuating the expression of C/EBPα, PPARγ, and SREBP-1c during the late phase of MDI-induced differentiation. In addition, p-coumaric acid increased the phosphorylation of AMPK and ACC, and the expression of carnitine palmitoyl transferase-1 (CPT-1) mRNA, in fully differentiated adipocytes, indicating that it promotes fatty acid β-oxidation via AMPK signaling. Taken together, our data suggest that SQE and p-coumaric acid might have the anti-obesitic effects via AMPK pathway in 3T3-L1 cells.
Phytotherapy Research | 2008
Soo-Youn Choi; Joon-Ho Hwang; Soo-Young Park; Yeong-Jun Jin; Hee-Chul Ko; Sang-Wook Moon; Se-Jae Kim
The goal of this study was to elucidate the antiinflammatory activities of Psidium guajava L. (guava) leaf. To improve the functionality of guava leaf, it was fermented with Phellinus linteus mycelia, Lactobacillus plantarum and Saccharomyces cerevisiae. The ethanol extract from fermented guava leaf inhibited lipopolysaccharide (LPS)‐induced nitric oxide (NO) and prostaglandin E2 (PGE2) production. Western blot analysis showed that fermented guava leaf extract decreased LPS‐induced inducible nitric oxide synthase (iNOS) and the cyclooxygenase‐2 (COX‐2) protein level in RAW 264.7 cells. To investigate the mechanism involved, the study examined the effect of fermented guava leaf extract on LPS‐induced nuclear factor‐κB (NF‐κB) activation. Fermented guava leaf extract significantly inhibited LPS‐induced NF‐κB transcriptional activity. Immunochemical analysis revealed that fermented guava leaf extract suppressed LPS‐induced degradation of I‐κBα. Taken together, the data indicate that fermented guava leaf extract is involved in the inhibition of iNOS and COX‐2 via the down‐regulation of NF‐κB pathway, revealing a partial molecular basis for the antiinflammatory properties of fermented guava leaf extract. Copyright
Biochemical and Biophysical Research Communications | 2008
Seong-Il Kang; Young-Jun Jin; Hee-Chul Ko; Soo-Youn Choi; Joon-Ho Hwang; Ilson Whang; Moo-Han Kim; Hye-Sun Shin; Hyung-Bok Jeong; Se-Jae Kim
The anti-diabetic potential of Petalonia binghamiae extract (PBE) was evaluated in vivo. Dietary administration of PBE to streptozotocin (STZ)-induced diabetic mice significantly lowered blood glucose levels and improved glucose tolerance. The mode of action by which PBE attenuated diabetes was investigated in vitro using 3T3-L1 cells. PBE treatment stimulated 3T3-L1 adipocyte differentiation as evidenced by increased triglyceride accumulation. At the molecular level, peroxisome proliferator-activated receptor gamma (PPARgamma) and terminal marker protein aP2, as well as the mRNA of GLUT4 were up-regulated by PBE. In mature adipocytes, PBE significantly stimulated the uptake of glucose and the expression of insulin receptor substrate-1 (IRS-1). Furthermore, PBE increased PPARgamma luciferase reporter gene activity in COS-1 cells. Taken together, these results suggest that the in vivo anti-diabetic effect of PBE is mediated by both insulin-like and insulin-sensitizing actions in adipocytes.
Phytotherapy Research | 2013
Seong-Il Kang; Hye-Sun Shin; Hee-Chul Ko; Se-Jae Kim
Sinensetin is a rare polymethoxylated flavone found in certain citrus fruits. In this study, we investigated the effects of sinensetin on lipid metabolism in mature 3T3‐L1 adipocytes. Sinensetin decreased the expression of sterol regulatory element‐binding protein 1c (SREBP1c), suggesting its antiadipogeneic property via downreguation of SREBP1c. Also, sinensetin increased the phosphorylation of protein kinase A and hormone‐sensitive lipase, indicating its lipolytic property via a cAMP‐mediated signaling pathway. Moreover, sinensetin inhibited insulin‐stimulated glucose uptake by decreasing the phosphorylation of insulin receptor substrate and Akt. Furthermore, sinensetin increased the phosphorylation of AMP‐activated protein kinase (AMPK) and acetyl‐CoA carboxylase. It also upregulated mRNA expression of carnitine palmitoyltransferase‐1a, suggesting that sinensetin enhances fatty acid β‐oxidation through the AMPK pathway. Taken together, these results suggest that sinensetin may have potential as a natural agent for prevention/improvement of obesity. Copyright
Nutrition Research | 2014
K.O. Kim; Yoo-Sun Kim; Ji Ye Lim; Soo Jin Min; Jae-Ho Shin; Hee-Chul Ko; Se-Jae Kim; Yunsook Lim; Yuri Kim
Sasa quelpaertensis leaves exert anti-inflammatory and anticarcinogenic effects, although it remains unclear whether these leaves can suppress inflammation-related intestinal diseases. This study hypothesized that Sasa quelpaertensis leaf extract (SQE) exerts a protective effect against inflammation in a dextran sulfate sodium (DSS)-induced colitis mouse model. Therefore, colon tissues of DSS-induced colitis mice that were treated with SQE were assayed for levels of proinflammatory markers, mitogen-activated protein kinase signaling, and activation of nuclear factor κB. For this purpose, mice were pretreated with SQE (100 mg/kg or 300 mg/kg body weight) by gavage for a 2-week period. Mice then received either SQE or sulfasalazine (100 mg/kg body weight) with 2.5% DSS in drinking water for 7 days twice daily and 7 days of tap water ad libitum between DSS treatment. Treatment with SQE was found to attenuate the severity of DSS-induced colitis, as assessed by disease activity index scores, shrinkage of colon length, and histopathologic changes. SQE reduced DSS-induced proliferation in distal colon tissues. It also significantly suppressed levels of tumor necrosis factor-α in serum and colon tissues, nitric oxide synthase, cyclooxygenase, and levels of phosphorylated c-Jun N-terminal kinases, p38, extracellular-signal-regulated kinases 1/2, and IκBα in colon tissues. To our knowledge, this is the first study to demonstrate that SQE supplementation can exert an anti-inflammatory effect on experimental chronic colitis.
Integrative Cancer Therapies | 2014
Mina Kim; Yoo-Sun Kim; K.O. Kim; Hee-Chul Ko; Se-Jae Kim; Jung-Hyun Kim; Yuri Kim
Lung cancer is the leading cause of cancer death worldwide, and most chemotherapeutic drugs have limited success in treating this disease. Furthermore, some drugs show undesirable side effects due to the enrichment of cancer stem cells (CSCs) that are present, leading to resistance to conventional chemotherapy and tumor relapse. CSCs possess self-renewal characteristics, aggressive tumor initiating activity, and ability to facilitate tumor metastasis. Therefore, development of nontoxic agents that can potentiate chemotherapy and eliminate CSCs would be highly desirable. In the present study, we investigated whether Sasa quelpaertensis leaf extracts (SQE) and cisplatin (CIS), individually or in combination, would exert anti-CSC and antimetastatic effect in H1299 and A549 human lung cancer cells. Following these treatments, cell growth, phosphorylation of phosphoinositide-3 kinase, and activation of the mammalian target of rapamycin were inhibited. Decreased serial sphere formation, clonogenicity, and expression of major stem cell markers, such as CD44 and SOX-2, in CD44+ cancer stem cells were also observed. In addition, inhibition of cell migration and invasion in both cell lines as well as inhibition of matrix metalloproteinase-2 activity and expression were detected. Importantly, the anticancer stemness and antimetastasis effects in each of these assays were greater for the combined treatment with SQE and CIS than with each treatment individually. In conclusion, the data suggest that SQE alone, or in combination with CIS, represents a promising therapeutic strategy for eliminating cancer stemness and cell invasion potential of CSCs, thereby treating and preventing metastatic lung cancer cells.