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传统医学养牛散和汤抑制3T3-L1细胞的脂肪生成并抑制过氧化物酶体增殖物激活受体γ的表达。

Traditional medicine yanggyuksanhwa-tang inhibits adipogenesis and suppresses proliferator-activated receptor-gamma expression in 3T3-L1 cells.

作者信息

Jeong Soo-Jin, Yoo Sae-Rom, Seo Chang-Seob, Shin Hyeun-Kyoo

机构信息

Herbal Medicine Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.

出版信息

Pharmacogn Mag. 2015 Jul-Sep;11(43):502-8. doi: 10.4103/0973-1296.160456.

Abstract

BACKGROUND

Yanggyuksanhwa-tang (YGSHT) is a specific traditional Korean herbal formula for Soyangin according to Sasang constitutional philosophy. Although its biological activities against inflammation and cerebral infarction have been reporting, there is no information about the adipogenic activity of YGSHT. In the present study, we investigated the anti-adipogenic activity of YGSHT to evaluate effects of YGSHT on adipogenesis in vitro.

MATERIALS AND METHODS

Using 3T3-L1 preadipocytes, we induced the cellular differentiation into adipocytes by adding insulin. Anti-adipogenic activity of YGSHT was measured by oil red O staining, triglyceride assay, glycerol-3-phosphate dehydrogenase (GPDH) activity test, and leptin assay.

RESULTS

YGSHT extract had no significant cytotoxicity in preadipocytes or differentiated adipocytes. YGSHT reduced the number of lipid droplets and content of triglyceride in adipose cells. YGSHT also significantly inhibited GPDH activity and decreased leptin production compared with control adipocytes. Down-regulation of peroxisome proliferator-activated receptor-gamma (PPAR-γ) expression at the messenger RNA level was observed in YGSHT-treated adipocytes.

CONCLUSION

Taken together, our data suggest that YGSHT has potential as an anti-obesity drug candidate.

摘要

背景

根据四象体质学说,羊角山和汤(YGSHT)是一种针对少阳人的特定传统韩国草药配方。尽管其抗炎和抗脑梗死的生物学活性已有报道,但关于YGSHT的脂肪生成活性尚无相关信息。在本研究中,我们研究了YGSHT的抗脂肪生成活性,以评估其在体外对脂肪生成的影响。

材料与方法

使用3T3-L1前脂肪细胞,通过添加胰岛素诱导细胞分化为脂肪细胞。通过油红O染色、甘油三酯测定、甘油-3-磷酸脱氢酶(GPDH)活性测试和瘦素测定来测量YGSHT的抗脂肪生成活性。

结果

YGSHT提取物在前脂肪细胞或分化的脂肪细胞中没有明显的细胞毒性。YGSHT减少了脂肪细胞中脂滴的数量和甘油三酯的含量。与对照脂肪细胞相比,YGSHT还显著抑制了GPDH活性并降低了瘦素的产生。在YGSHT处理的脂肪细胞中观察到信使核糖核酸水平上的过氧化物酶体增殖物激活受体γ(PPAR-γ)表达下调。

结论

综上所述,我们的数据表明YGSHT有潜力成为一种抗肥胖药物候选物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a555/4522835/c499dd3f1dc6/PM-11-502-g003.jpg

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