• 대한화장품학회지
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• 제49권2호
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• pp.97-106
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• 2023

본 연구에서는 사이클로덱스트린을 함유하여 고함량 세라마이드 제형 안정화 연구를 하고자 한다. 인체 피부 장벽인 세포간지질을 구성하는 세라마이드는 피부 속 수분을 보호하고 피부 장벽을 강화함으로써 보습유지에 매우 중요한 성분이다. 그러나 세라마이드는 난용성이므로 화장품 제형에 포함되었다 하더라도 서서히 겔화(gelation) 또는 결정화(crystallization)되어 경시적으로 석출되는 치명적인 문제점을 갖고 있어 고함량 처방하는 데 어려움이 있다. 사이클로덱스트린은 글루코오스 분자가 연결된 환형 올리고당으로 그 외부 표면은 친수성이고 내부는 소수성인 원통형 구조를 가지고 있어 난용성 약물의 용해성 개선 및 흡수성의 개선 등 약물의 물리화학적인 성질을 개선시키는 것으로 알려져 있다. 본 연구진은, 사이클로덱스트린을 활용하여 세라마이드 안정화 제형 실험 후 경도 측정 및 편광 현미경 관찰을 통해 세라마이드 석출 여부를 확인하였다. 본 연구 결과 사이클로덱스트린을 함유한 고함량 세라마이드 제형이 세라마이드의 겔화 또는 결정화를 예방하여 석출을 방지하는 효과가 있어 제형 안정성, 환경 조건별 보관 안정성 및 피부 보습력이 우수한 효과가 있다는 것을 확인하였다.

• Molecules and Cells
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• 제38권6호
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• pp.482-495
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• 2015

Sphingolipids such as ceramide, sphingosine-1-phosphate and sphingomyelin have been emerging as bioactive lipids since ceramide was reported to play a role in human leukemia HL-60 cell differentiation and death. Recently, it is well-known that ceramide acts as an inducer of cell death, that sphingomyelin works as a regulator for microdomain function of the cell membrane, and that sphingosine-1-phosphate plays a role in cell survival/proliferation. The lipids are metabolized by the specific enzymes, and each metabolite could be again returned to the original form by the reverse action of the different enzyme or after a long journey of many metabolizing/synthesizing pathways. In addition, the metabolites may serve as reciprocal biomodulators like the rheostat between ceramide and sphingosine-1-phosphate. Therefore, the change of lipid amount in the cells, the subcellular localization and the downstream signal in a specific subcellular organelle should be clarified to understand the pathobiological significance of sphingolipids when extracellular stimulation induces a diverse of cell functions such as cell death, proliferation and migration. In this review, we focus on how sphingolipids and their metabolizing enzymes cooperatively exert their function in proliferation, migration, autophagy and death of hematopoetic cells, and discuss the way developing a novel therapeutic device through the regulation of sphingolipids for effectively inhibiting cell proliferation and inducing cell death in hematological malignancies such as leukemia, malignant lymphoma and multiple myeloma.

• 한국해양바이오학회지
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• 제4권1호
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• pp.31-34
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• 2010

The primary function of the skin is to protect the body from the unwanted environmental influences. The outermost layer of the skin is stratum corneum which consists of corneocytes surrounded by lipid regions. Ceramides covalently bound to keratinocytes are essential for the barrier function of the skin, which can be disturbed in the disease, like xerosis. Xerosis is an abnormal dryness of the skin which reduced the thickness of stratum corneum and ceramide content decreasing with age. In this study, 36 seaweed extracts have been tested for screening of xerosis inhibitory agent by in vitro HaCaT keratinocyte assay. Ishige sinicola and Helminthocladia australis induced the significant amount of ceramide-like substance I in HaCaT keratinocyte among the tested seaweed extracts. Sargassum fulvellum, Chondrus ecellatus and Gigartina tenella also induced the ceramide-like substance I whereas Helminthocladia australis and Pachymeniopsis elliptica induced the ceramide-like II from HaCaT keratinocyte.

• BMB Reports
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• 제50권3호
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• pp.144-149
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• 2017

Ceramides are the major sphingolipid metabolites involved in cell survival and apoptosis. When HepG2 hepatoma cells were treated with celecoxib, the expression of the genes in de novo sphingolipid biosynthesis and sphingomyelinase pathway was upregulated and cellular ceramide was elevated. In addition, celecoxib induced endoplasmic reticulum (ER) stress in a time-dependent manner. SPTLC2, a subunit of serine palmitoyltransferase, was overexpressed by adenovirus. Adenoviral overexpression of SPTLC2 (AdSPTLC2) decreased cell viability of HEK293 and HepG2 cells. In addition, AdSPTLC2 induced apoptosis via the caspase-dependent apoptotic pathway and elevated cellular ceramide, sphingoid bases, and dihydroceramide. However, overexpression of SPTLC2 did not induce ER stress. Collectively, celecoxib activates de novo sphingolipid biosynthesis and the combined effects of elevated ceramide and transcriptional activation of ER stress induce apoptosis. However, activation of de novo sphingolipid biosynthesis does not activate ER stress in hepatoma cells and is distinct from the celecoxib-mediated activation of ER stress.

• 대한한의학회지
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• 제42권4호
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• pp.197-207
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• 2021

Objectives: The purpose of this study was to confirm effect of reducing inflammation of Coptis chinensis extract-ceramide complex through the endocannabinoid system (ECS) control in atopic dermatitis. Methods: 8-week-old ICR mice were divided into normal group (Ctrl), lipid barrier elimination group (ADE), palmitoylethanolamide treated group after lipid barrier elimination (PEAT), and Coptis chinensis extract-ceramide complex applied group after lipid barrier elimination (CRA). After inducing atopic dermatitis, cannabinoid receptor (CB) 1, CB2, CD68, p-I𝜅B, iNOS, substance P and serotonin were observed to confirm the regulation of the ECS, macrophage activity and mast cell activity. Results: CB1 and CB2 showed higher positive reactions in the CRA than in the ADE and PEAT. CD68, p-I𝜅B and iNOS showed higher positive reaction in the ADE, PEAT and CRA than in the Ctrl, but the increase in the positive reaction was lower in the CEA compared to the ADE and PEAT. Substance P and serotonin showed higher positive reaction in the ADE, PEAT and CRA than in the Ctrl, but the increase in the positive reaction was lower in the CEA compared to the ADE and PEAT. Conclusions: The effects of Coptis chinensis extract -ceramide complex were confirmed on the regulation of the ECS, macrophage activity and mast cell activity.

• Archives of Pharmacal Research
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• 제26권4호
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• pp.270-274
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• 2003

A series of new 3-alkyl-1-(1-methyl-2-phenylethyl)ureas related to ceramide was synthesized and evaluated for their in vitro cytotoxic activity against five human tumor cell lines. The urea analogue (2b) of 813 showed comparable or slightly more potent cytotoxic activity as compared to B13, indicating that urea does appear to serve as a bioisostere of amide.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 춘계학술대회 논문집
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• pp.50-50
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• 2003

Nitric oxide (NO) has been studied and found to be an important intracellular modulator. The excess NO produced by the inducible nitric-oxide synthase (iNOS) is implicated in various inflammatory diseases and cellular injury. Inflammatory cytokines such as TNF- or IL-6 increase intracellular ceramide and ceramide may induce NO production and inflammation. (omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.156.1-156.1
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• 2003

Cerarmide acts as a lipid second messenger in the cellular signal transduction and is involved in mediating a variety of cell functions such as proliferation, differentiation, growth arrest, and apoptosis. In the present study, we have investigated the effect of ceramide on cellular cytotoxity and reactive oxygen species (ROS) to understand the relationship between them. Ceramide treatment significantly increased cell death in RAW 264.7 murine macrophages activated with lipopolysaccharide (LPS) and interferon-g (IFN-g). (omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.279.1-279.1
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• 2002

Accumulation of ceramide mass in MCF-7 cells by the anti-cancer agent. paclitaxel. was found to occur primarily due to activation of the de novo synthesis pathway. Morever. the addition of paclitaxel resulted in the accumulation of ceramide, which was followed by a prolonged arachidonic acid release. Participation of ceramide de novo pathway in arachidonate signaling was detected since L-cycloserine, an inhibitor of de novo synthesis, was able to inhibit the paclitaxel-induced AA release and cytotoxicity. (omitted)

• BMB Reports
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• 제37권2호
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• pp.192-198
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• 2004

The hepatitis C virus (HCV) core protein is believed to be one of viral proteins that are capable of preventing virus-infected cell death upon various stimuli. But, the effect of the HCV core protein on apoptosis that is induced by various stimuli is contradictory. We examined the possibility that the HCV core protein affects the ceramide-induced cell death in cells expressing the HCV core protein through the sphingomyelin pathway. Cell death that is induced by $C^2$-ceramide and bacterial sphingomyelinase was analyzed in 293 cells that constitutively expressed the HCV core protein and compared with 293 cells that were stably transfected only with the expression vector. The HCV core protein inhibited the cell death that was induced by these reagents. The protective effects of the HCV core protein on ceramide-induced cell death were reflected by the reduced expression of $p21^{WAF1/Cip1/Sid1}$ and the sustained expression of the Bcl-2 protein in the HCV core-expressing cells with respect to the vector-transfected cells. These results suggest that the HCV core protein in 293 cells plays a role in the modulation of the apoptotic response that is induced by ceramide. Also, the ability of the HCV core protein to suppress apoptosis might have important implications in understanding the pathogenesis of the HCV infection.