• Proceedings of the Botanical Society of Korea Conference
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• 1985.08b
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• pp.83-96
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• 1985

cDNAs for long- and short-chain acyl-CoA oxidases in fatty acid $\beta$-oxidation were isolated and were characterized their enzymatical and molecular properties. Both oxidases were exclusively localized in glyoxysomes, indicating that glyoxysomes can completely metabolize fatty acids to acyl-CoA by their cooperative action. In order to clarify the regulatory mechanisms underlying degradation of storage oil, we tried to obtain glyoxysome-deficient mutants of Arabidopsis. We screened 2,4-dichlorophenoxybutyric acid (2,4-DB) mutants of Arabidopsis which have defects in glyoxysomal fatty acid $\beta$-oxidation. Four mutants can be classified as carrying alleles at three independent loci, which we designated pedl, ped2, and ped3, respectively (where ped stands for peroxisome defective). The characteristics of these ped mutants are described.

• Archives of Pharmacal Research
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• v.28 no.2
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• pp.142-150
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• 2005

The synthesis and structure-activity relationships of a novel series of substituted quercetins that activates peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) are reported. The $PPAR{\gamma}$ agonistic activity of the most potent compound in this series is comparable to that of the thiazolidinedione-based antidiabetic drugs currently in clinical use.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2001.10b
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• pp.116-117
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• 2001

• Archives of Pharmacal Research
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• v.29 no.5
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• pp.394-399
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• 2006

Benzothiazole derivatives of thiazolidinediones (TZD) were synthesized using a modified Mitsunobu reaction of 2-(benzothiazol-2-ylmethylamino)ethanol (2) with 5-(4-hydroxybenzyl)-3-triphenylmethylthiazolidine-2,4-dione and assayed for activity on peroxisome proliferator-activated receptor (PPAR) subtypes and inhibitory activity of NO production in lipopolysaccharide-activated macrophages. Most of the tested compounds were identified as potent $PPAR_\gamma$ agonists, indicating their potential as drug candidates for diabetes.

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.194.1-194.1
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• 2001

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.187.1-187.1
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• 2003

Type 2 diabetes is characterized by high level of blood glucose and insulin and impaired action. In recent years, the treatment of type 2 diabetes has been revolutionized with the advent of thiazolidinedione (TZD) class of molecules that ameliorate insulin resistance and thereby normalize elevated blood glucose levels. These TZDs are synthetic, high-affinity ligands of peroxisome proliferator activated receptor-gamma (PPAR${\gamma}$); a member of the nuclear receptor family that controls the expression of genes in the target tissues of insulin action. (omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.110-110
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• 2002

15-Deoxy-$\Delta$12, 14-prostaglandin J2 (15-deoxy-PGJ2), a naturally occurring ligand activates the peroxisome proliferator-activated receptor-$\gamma$(PPAR-$\gamma$). It was known to have promoting ability of nerve growth factor(NGF)-induced neurite extension. However, it is not clear yet as to what signaling pathway is involved in its promoting ability of neurite extension.(omitted)

• Journal of Life Science
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• v.21 no.5
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• pp.647-655
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• 2011

The neurotoxicity of aggregated amyloid ${\beta}$ ($A{\beta}$) has been implicated as a critical cause in the pathogenesis of Alzheimer's disease (AD). It can cause neurotoxicity in AD by evoking a cascade of apoptosis to neuron. Here, we investigated the neuroprotective effects of cilostazol, which acts as a phosphodiesterase III inhibitor, on $A{\beta}_{25-35}$-induced cytotoxicity in mouse neuronal cells and cognitive decline in the C57BL/6J AD mouse model via peroxisome proliferator-activated receptor (PPAR)-${\gamma}$ activation. $A{\beta}_{25-35}$ significantly reduced cell viability and increased the number of apoptotic-like cells. Cilostazol treatment recovered cells from $A{\beta}$-induced cell death as well as rosiglitazone, a PPAR-${\gamma}$ activator. These effects were suppressed by GW9662, an antagonist of PPAR-${\gamma}$ activity, indicative of a PPAR-${\gamma}$-mediated signaling. In addition, cilostazol and rosiglitazone also restored PPAR-${\gamma}$ activity levels that had been altered as a result of $A{\beta}_{25-35}$ treatment, which were antagonized by GW9662. Furthermore, cilostazol also markedly decreased the number of apoptotic-like cells and decreased the Bax/Bcl-2 ratio. Intracerebroventricular injection of $A{\beta}_{25-35}$ in C57BL/6J mice resulted in impaired cognitive function. Oral administration of cilostazol (20 mg/kg) for 2 weeks before $A{\beta}_{25-35}$ injection and once a day for 4 weeks post-surgery almost completely prevented the $A{\beta}_{25-35}$-induced cognitive deficits, as did rosiglitazone. Taken together, our findings suggest that cilostazol could attenuate $A{\beta}_{25-35}$-induced neuronal cell injury and apoptosis as well as promote the survival of neuronal cells, subsequently improving cognitive decline in AD, partly because of PPAR-${\gamma}$ activation. The phosphodiesterase III inhibitor cilostazol may be the basis of a novel strategy for the therapy of AD.

• Journal of Life Science
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• v.22 no.12
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• pp.1688-1696
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• 2012

Oenanthe javanica has been used as a food source and also in traditional folk medicine for its detoxifying properties and anti-microbial effects since ancient times. In this study, we evaluated the effect and mechanism of O. javanica seed methanol extract (OJSE) on adipocyte differentiation by 3T3-L1 preadipocytes. Under non-toxic conditions, OJSE treatment resulted in a dose-dependent inhibition of lipid droplet generation and triglyceride accumulation by suppressing adipocyte differentiation, which are associated with the decreased expression of key proadipogenic transcription factors including CCAAR/enhancer binding protein ${\alpha}$, ${\beta}$ ($C/EBP{\alpha}$, $C/EBP{\beta}$) and peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$). OJSE also significantly inhibited proliferation and differentiation of 3T3-L1 preadipocytes through G1-phase arrest, indicating that OJSE blocked mitotic clonal expansion during adipocyte differentiation. Investigation of the alteration of G1 phase arrest-related proteins indicated a dose-dependent increase in the expression of p21 and reduction in expression of cyclin E, Cdk2, E2F-1 and phospho-Rb by OSJE. Taken together, these results suggest that OJSE inhibits adipocyte differentiation by blocking the mitotic clonal expansion, which is accompanied by preadipocyte cell cycle arrest.

• Journal of Life Science
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• v.28 no.7
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• pp.857-863
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• 2018

This study examined whether the supplementation of Salicornia herbacea L. (SH), a member of the Chenopodiaceae subfamily, affects tissue specific triglyceride (TG) accumulation and the peroxisome proliferator-activated $receptor-{\gamma}$ $coactivator-1{\alpha}$ ($PGC-1{\alpha}$) and peroxisome proliferator-activated $receptor-{\gamma}$ ($PPAR-{\gamma}$) protein expressions of skeletal muscle in rats with a high-fat diet. Sprague-Dawley male rats were randomly divided into three groups: control normal diet group (CD), high-fat diet group (HD), and 5.0% SH supplemented high-fat diet group (SD). The weights of fat tissue of the SD group were reduced by approximately 25%(p<0.01), while the skeletal muscle weight of the SD group increased approximately 5% compared to those in the HD group (p<0.01). The serum and hepatic TG of the SD group decreased approximately 20% compared to those of the HD group (p<0.05). In the protein expression levels in the skeletal muscle, the $PGC-1{\alpha}$ and $PPAR-{\gamma}$ expressions of the SD group were 1.5-folds higher than those of the HD group (p<0.01). From these results, SH supplementation contributes to the improvement of the serum and hepatic TG concentrations, and the $PGC-1{\alpha}$ and $PPAR-{\gamma}$ protein expression levels in the skeletal muscle of fed a high-fat diet. Thus, SH supplementation was effective in reducing fat mass and increasing muscle mass.