PPARα activator가 고지방 사료를 섭취한 운동하지 않은 쥐에 비해 고지방 사료를 섭취한 운 동 쥐에서 백색지방조직의 혈관신생을 보다 효과적으로 억제하는지를 조사하였다. 수컷 쥐는 무작위로 PPARα activator인 fenofibrate와 운동을 모두 처리하지 않은 대조군(Con), fenofibrate 단독처리군(FF), 운동 단독처리군(Ex) 및 fenofibrate와 운동의 조합처리군(Ex+FF)으로 나누어 8주간 고지방 사료를 섭취시 켰다. 백색지방조직의 무게와 백색지방세포의 크기는 Con에 비해 FF, Ex 및 Ex+FF 모두 감소하였으며, Ex+FF는 FF에 비해 더욱 감소하였다. 백색지방조직에서 MMPs와 혈관신생 인자의 유전자 발현은 Con에 비해 FF, Ex 및 Ex+FF 모두 감소하였으며, Ex+FF는 FF에 비해 더욱 감소하였다. 그러나 혈관신생 억제인 자의 유전자 발현은 Con에 비해 FF, Ex 및 Ex+FF 모두 증가하였고, Ex+FF는 FF에 비해 더욱 증가하였 다. 따라서 본 연구는 fenofibrate 단독처리보다는 fenofibrate와 운동의 조합처리가 효과적으로 백색지방조 직의 혈관신생을 억제함으로써 백색지방조직의 증가를 감소시키고 복부비만을 억제한다는 것을 밝혔다.

The root of Paeonia lactiflora has been used in Chinese medicine. We conducted to check the comparative qualities of ethanol solvent extraction (PLE) and supercritical carbon dioxide extraction (PLS) of P. lactiflora root. PLE had higher antioxidant and polyphenol contents than PLS. But, PLS were significantly increased peroxisome proliferator-activated receptor (PPAR)-α. In addition, PLS inhibited the adipocyte differentiation of 3T3-L1 cells. When treated with the extract at a concentration of 100 μg/mL, the Wnt/β-catenin pathway reporter luciferase activity of HEK 293-TOP cells increased approximately by 3-folds compared to that of the untreated control group. These results indicate that P. lactiflora supercritical carbon dioxide extract may serve as a cosmeceutical for improving skin barrier function and the treatment of obesity.

Background : Obesity, a global health problem and a chronic diseases, is associated with increased risk of developing type 2 diabetes and coronary heart diseases. A wide variety of natural remedies have been explored for their obesity treatment potential. To elucidate the anti-obesity effect of ginsenoside Rg5 : Rk1 (Rg5 : Rk1), a mixture of protopanaxadiol type ginsenosides isolated from Panax ginseng Meyer in a 3T3-L1 adipocytes. Methods and Results : In order to determinate the anti-obesity effect of Rg5 : Rk1, Oil Red O staining and triglyceride (TG) content was assessed. Furthermore, to elucidate the possible mechanism whether Rg5:Rk1 affects lipid accumulation, mRNA and protein expression analyses of adipocyte markers such as STAT3, PPARγ, CBEPα and ap2 were carried out. Rg5:Rk1 treatment showed an inhibition of lipid droplet accumulation and decrease on TG content. In addition, expression of STAT3, PPARγ, CEBPα and ap2 were decreased in dose dependent manner. Similar to these results, Rg5:Rk1 treatment reduced PPARγ and CEBPα protein expression. Conclusion : Rg5 : Rk1 treatment exhibits anti-adipogenic activity by down-regulation of the STAT3PPARγ/CEBPα pathway in 3T3-L1 adipocyte cell line.

Background : Non-alcoholic fatty liver disease (NAFLD) is caused by obesity, type 2 diabetes mellitus, dyslipidemia, and genetic factors. Also, hyperinsulinemia directly promotes fat accumulation in hepatocytes. Therefore, it is very important to suppress the most common risks of NAFLD, such as obesity and insulin resistance. In this context, we evaluated for the effects of black ginseng (BG) extract on lipid accumulation inhibition and degradation in hepatocytes. Methods and Results : The aim of this study is to figure out the potential anti-lipogenic effects and the underlying mechanism of BG extract in a cellular-, type 2 diabetes mellitus (T2DM) animal model associated with NAFLD. T2DM animal used C57BL/KsJ db/db mouse (M. 6 wk, n = 56), treated with extract of BG and Red ginseng (RG) (each 100 and 900 ㎎/ ㎏/day, p.o) for 6 weeks. BG markedly reduced palmitate-induced intracellular lipid accumulation in HepG2 cells. On histology of liver tissues of T2DM animal, macrovesicular lipid droplets in cytoplasm of hepatocytes were decreased both RG and BG-treated groups. In liver tissue, BG-treated groups suppressed CCAAT/enhancer binding protein-α (C/EBP-α), sterol regulatory element-binding protein-1c (SREBP-1c) expression, and SREBP-1c mediated induction of acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) proteins related to the induction of adipose differentiation. Futhermore, adenosine monophosphate (AMP)-activated protein kinase (AMPK) activity was significantly increased in BG-treated groups compared to RG-treated groups. It is also found that peroxisome proliferator-activated receptor-α (PPAR-α) highly expressed in BG-treated groups. Conclusion : Our results suggest that black ginseng extract has an anti-adipogenic and anti-lipogenic effects in the liver when administered as a food supplement and has potential as a therapeutic agent for obesity and T2DM induced NAFLD.

자외선은 피부 노화를 가속화하여 피부 광노화를 유발하고, 일광 화상, 피부암 등을 유발한다. 자외선 차단제를 사용하더라도 일부 자외선에 의하여 피부 손상은 유발될 수 있기 때문에 자외선에 대한 피부 자체의 방어력을 올려주는 것이 필요하다. 최근, 식물에서 자외선 보호 기능을 하는 것으로 알려진 COP1이 사람의 피부 에서도 자외선에 대한 반응들을 조절한다고 새롭게 밝혀졌다. 본 연구에서는, COP1과 그의 결합 단백질 DET1 이 사람 피부의 각질형성세포에서 자외선에 대한 시그날 조절 물질인 c-Jun 단백질 양을 조절하는 것을 확인하 였다. 자외선에 노출 시 COP1과 DET1 발현이 감소하였고, 그 영향으로 c-Jun 단백질이 증가하였다. 반대로 COP1과 DET1을 발현하는 DNA를 transfection 시켜줄 경우 c-Jun 단백질 양이 감소하였다. 피부 각질형성 세포에서 COP1과 DET1의 발현을 조절할 수 있는 물질을 탐색한 결과, 초피나무 열매 추출물이 COP1과 DET1의 발현을 증가시켜 주었다. 초피나무 열매 추출물은 c-Jun 시그날에 의해서도 조절되는 MMP1이 자외 선에 의해 유도되는 것을 억제하였다. 뿐만 아니라, 초피나무 열매 추출물 PPAR-α 활성이 있어 장벽강화를 통한 피부 보호 효과가 있는데, 자외선에 의하여 염증 유발 물질인 IL-6와 IL-8의 발현이 증가하는 것도 억제 하였다. 사람의 팔에 자외선을 쪼여 준 경우에도 초피나무 열매 추출물이 홍반이 생기는 것을 억제하고 홍반에 의한 색소침착도 억제하였다. 종합적으로, 초피나무 열매 추출물은 다양한 메카니즘을 통하여 자외선으로부터 피부를 보호해 줄 것으로 기대된다.

In particular, maternal prostacyclin (PGI2) is critical for embryo implantation and the action of PGI2 is not mediated via its G protein-coupled membrane receptor, IP, but its nuclear receptor, peroxisome proliferator-activated receptor δ (PPARδ). Recently, several studies have shown that PGI2 enhances blastocyst development and/or hatching rate in vitro, and subsequently implantation and live birth rates in mice. However, the mechanism by which PGI2 improves preimplantation embryo development in vitro remains unclear. Using molecular, pharmacologic and genetic approaches, we show that PGI2-induced PPARδ activation accelerates blastocyst hatching in mice. mRNAs for PPARδ, RXRs (heterodimeric partners of PPARδ) and PGI2 synthase are temporally induced after zygotic gene activation and their expression reaches maximum levels at the blastocyst stage, suggesting that functional complex of PPARδ can be formed in the blastocyst. Carbaprostacyclin (cPGI, a stable analogue of PGI2) and GW501516 (a PPARδ selective agonist) significantly accelerated blastocyst hatching but did not increase total cell number of cultured blastocysts. Whereas U51605 (a PGIS inhibitor) interfered with blastocyst hatching, GW501516 restored U51605-induced retarded hatching. In contrast to improvement of blastocyst hatching by PPARδ agonists, PPAR antagonists significantly inhibited blastocyst hatching. Furthermore, deletion of PPARδ at early stages of preimplantation mouse embryos caused delay of blastocyst hatching, but did not impair blastocyst development. Taken together, PGI2-induced PPARδ activation accelerates blastocyst hatching in mice.