• Biomolecules & Therapeutics
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• v.13 no.1
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• pp.7-12
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• 2005

GyeongshinhaeGihwan T1 (GGT1) is a newly developed oriental medicine to help weight control. We investigated nitric oxide production and cytokine secretion in mouse peritoneal macrophages. According to recent reports, macrophages are participated in fat accumulation and closely related with obesity. In this study, using mouse peritoneal macrophages, we have examined whether GGT1 affects the production of nitric oxide (NO), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), and interleukin (IL)-12 by the stimulation of interferon-${\gamma}$ and lipopolysaccharide (LPS). GGT1 inhibits LPS-induced NO production in a dose-dependent manner. The decrease in NO synthesis was reflected as a decreased amount of inducible NO synthese protein. We also found that GGT1 inhibits pro-inflammatory cytokines, TNF-${\alpha}$ and IL-12 production. In mouse embryo preadipocyte 3T3-L1, GGT1 reduced the viability in a dose-dependent manner. These findings suggest that GGT1 may have potential effects in preventing and controlling adipogenesis and obesity.

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.136.1-136.1
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• 2002

• Asian-Australasian Journal of Animal Sciences
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• v.29 no.11
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• pp.1646-1652
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• 2016

Mammalian target of rapamycin complex 1 (mTORC1) is a central regulator of cell growth and metabolism and is sufficient to induce specific metabolic processes, including de novo lipid biosynthesis. Elongation of very-long-chain fatty acids 1 (ELOVL1) is a ubiquitously expressed gene and the product of which was thought to be associated with elongation of carbon (C) chain in fatty acids. In the present study, we examined the effects of rapamycin, a specific inhibitor of mTORC1, on ELOVL1 expression and docosahexaenoic acid (DHA, C22:6 n-3) synthesis in bovine mammary epithelial cells (BMECs). We found that rapamycin decreased the relative abundance of ELOVL1 mRNA, ELOVL1 expression and the level of DHA in a time-dependent manner. These data indicate that ELOVL1 expression and DHA synthesis are regulated by mTORC1 in BMECs.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.422.1-422.1
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• 2002

This study examined the pharmacokinetic disposition of SJ-8029. a novel anticancer agent possessing microtubule and topoisomerase inhibiting activities. in mice. rats. rabbits and dogs after i.v. administration. The serum concentration-time curves of SJ-8029 were best described by tri-exponential equations in all these animal species. The mean CI. $V_{ss}$ and $t_{1/2}$ were 0.3 L/h. 0.1 Land 63.2 min in mice. 1.5 L/h. 1.6 Land 247.7 min in rats. 13.8 L/h. 39.6 Land 245.9 min in rabbits. and 29.2 L/h. 44.6 Land 117.4 min in dogs. respectively. (omitted)

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.269.1-269.1
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• 2000

• Proceedings of the PSK Conference
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• 2000.04a
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• pp.150.1-150.1
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• 2000

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.176.1-176.1
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• 2001

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.184.1-184.1
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• 2001

• Korean Journal of Veterinary Research
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• v.63 no.2
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• pp.1.1-1.1
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• 2023

• Archives of Pharmacal Research
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• v.28 no.10
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• pp.1177-1182
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• 2005

The hepatotoxic effects of 1-bromopropane (1-BP) and its conjugation with glutathione were investigated in male ICR mice. A single dose (1000 mg/kg, po) of 1-BP in corn oil to mice significantly increased serum activities of alanine aminotransferase and aspartate aminotransferase. Glutathione (GSH) content was dose-dependently reduced in liver homogenates 12 h after 1-BP treatment. In addition, 1-BP treatment dose-dependently increased levels of S-pro-pyl GSH conjugate at 12 h after treatment, as measured by liquid chromatography-electro-spray ionization tandem mass spectrometry. The GSH conjugate was maximally increased in liver at 6 h after 1-BP treatment (1000 mg/kg), with a parallel depletion of hepatic GSH content. Finally, 1-BP induced the production of malondialdehyde in liver. The present results suggest that 1-BP might cause hepatotoxicity, including lipid peroxidation via the depletion of GSH, due to the formation of GSH conjugates in male ICR mice.