|摘要: ||肥胖症是一種已開發國家的健康問題。肥胖 (Obesity ) 是一種能量代謝疾病，通常伴隨著一些常見的文明病，如第二型糖尿病、高血壓及血脂異常 ( dyslipidemia ) 等。本研究係以丹參三種不同萃取物進行實驗，包括〔熱水(HWESM)、酒精(EESM)及二氧化碳超臨界(SCESM-5)〕萃取物，結果證實丹參二氧化碳超臨界萃取物 ( SCESM-5 )對 3T3-L1 細胞有抑制細胞增生的效力最佳。細胞經 SCESM-5 作用24小時，SCESM-5 會誘導ROS生成，顯示細胞週期停滯在S期並發現會降低G0/G1期之表現，其結果呈劑量效應。SCESM-5具有降調節 Bcl-2 與 PPAR-γ蛋白質，並且升調節 CD95(APO-1/CD95)、Bax、AMPK及 p-AMPK 蛋白質，同時PARP亦出現裂解，其結果皆呈現劑量與時間效應。除此之外，細胞經 SCESM-5 作用後，ERK 及 JNK 會活化及磷酸化。綜合上述結果顯示 SCESM-5 對 3T3-L1 前趨脂肪細胞具有抗細胞增生之效力，其作用機制可能是透過 CD95 ( APO-1/CD95 ) 系統及 AMPK 路徑調節之影響。|
Obesity has been a health problem in developed countries. It is a metabolic disease that usually occurs with diseases such as Type 2 diabetes mellitus, hypertension and dyslipidemia. Salvia miltiorrhiza which belongs to the Labiatae family, has been widely used in Chinese traditional medicine. It is a folk treatment for heart disease, hepatitis, haemorrhage, menstrual disorders, miscarriage, oedema, and insomnia, and recent data suggest its utility for substance dependence. In this study, our objectives were to examine the anti-proliferative properties of different Salvia miltorrhiza ( SM ) extract 〔i.e. equeous ( HWESM ), ethanolic ( EESM ) and supercritical carbon dioxide ( SCESM-5 )〕in 3T3-L1 adipocytes. Results showed that compared with HWESM and EESM, SCESM-5 demonstrated the most potent inhibitory effect on 3T3-L1 cell proliferation and cell cycle progression. After 24 h of treatment, SCESM-5 induced the generation of reactive oxygen species ( ROS ), displayed cell cycle arrest at S phase and was found to decrease in G0/G1 phase in a dose-dependent pattern. It also down-regulated the Bcl-2 and PPAR-γ proteins, and up-regulated the CD95 ( APO-1/CD95 ), Bax, AMPK and p-AMPK proteins, as well as cleaving the poly ( ADP-ribose ) polymerase ( PARP ) protein in a dose- and time-dependent manner. Furthermore, both the ERK and JNK were activated and phosphorylated after SCESM-5 treatment. Taken together, the present study indicates that SCESM-5 possesses potent anti-proliferative effects on 3T3-L1 adipocytes, and its mechanisms of action could be mediated through the CD95 ( APO-1/CD95 ) system and AMPK pathway.