Saururus chinensis Lour Baill Saururaceae a perennial herb i

Saururus chinensis (Lour.) Baill. (Saururaceae), a perennial herb, is widely cultivated in China and southern Korea. It has been traditionally used as folk medicine for the treatment of inflammation, jaundice and gonorrhea [8]. Previous chemical studies of S. chinensis have revealed the presence of lignans [9], flavonoids [10] and alkaloids [11]. Sauchinone, a lignan isolated from S. chinensis with unique structure, exhibited a great many pharmacological activities including anti-inflammatory [12], hepatoprotective [13], antidiabetic [14], and antioxidant effects [15] in various cell types. As a part of our exploration on the traditional medicine, S. chinensis was studied, which resulted in the isolation of two new sauchinone analogues (1–2) along with eight known compounds (3–10) (Fig. 1). Herein we reported the isolation, structural elucidation of two new lignans and evaluation of DGAT inhibitory activity about these isolates.
Experimental
Acknowledgments This research was financially supported by the Project Sponsored by the State Education Ministry, Key Laboratory of Natural Resources of Changbai Mountain & Functional Molecules (201305, Yanbian University, Ministry of Education of the People\'s Republic of China), Special Funds of Medical Programmes of Jilin Province (YYZX201240), the Development and Reform Commission of Jilin Province (20111439), and (2013G020).
Introduction Obesity and type 2 diabetes have been on a dramatic rise in Westernized countries over the last few decades, resulting in substantial societal burdens. The increased prevalence of these conditions is largely driven by a net imbalance between 50014 synthesis intake and expenditure. This in turn results in a net increase in fat disposition resulting from excess storage of triglycerides. The resulting increases in triglyceride stores in peripheral tissues, especially skeletal muscle, have been implicated in the development of insulin resistance and the constellation of lipotoxic disorders associated with metabolic syndrome X. Intracellular concentrations of lipids in muscle have been shown to be tightly, negatively correlated with insulin-stimulated glucose disposal in healthy males. This relationship is also found in humans with impaired glucose tolerance and type 2 diabetes. An additional line of evidence supporting the lipotoxicity hypothesis is the metabolic state of individuals suffering from the genetic disorders leading to lipodystrophy. Lipodystrophy is characterized by the absence of fat tissue, however, these individuals have excessive accumulation of lipids in metabolic tissues such as skeletal muscle and the liver. This aberrant distribution of lipids leads to an extreme insulin-resistant state. In animal models of lipodystrophy, treatment with the adipose regulatory hormone leptin reduces intracellular lipid levels in skeletal muscle and other tissues, leading to improved insulin sensitivity.6, 7 Given this critical role of lipid burden, oral therapies that have the potential to reverse this state hold significant potential in the treatment of type 2 diabetes, obesity and metabolic syndrome X. The enzymes involved in lipid biosynthesis pathways have attracted considerable interest as potential targets for disruption of aberrant lipid accumulation and its resulting impact on a range of disease states.8, 9 Triglyceride biosynthesis and the resulting lipid burden placed on tissues are largely controlled by two major pathways in humans. The monoacylglyceride pathway is typically operative in tissues where dietary monoacylglycerides are reesterified, such as small intestine, liver and adipose. Fatty acids that enter this pathway come from dietary absorption or via de novo fatty acid synthesis from acetyl CoA, via a series of enzyme-catalyzed homologation reactions. The second pathway, found in most cell types, is the glycerol phosphate pathway which sequentially adds two fatty acyl chains to glycerol-3-phosphate generating a phosphatidic acid intermediate that is subsequently converted to triglycerides. Both of these pathways converge at intermediate diacylglycerols which are then converted to triglycerides through acylation by a fatty acid acyl-CoA, catalyzed by acyl-CoA:diacylglycerol acyltransferases (DGAT). This family of enzymes is composed of DGAT-1 and DGAT-2, which while they carry out the same biotransformation, arise from divergent gene families.12, 13, 14 Consistent with the lipotoxicity hypothesis, mice lacking DGAT-1 (DGAT-1−/−) are resistant to diet-induced obesity and have increased insulin sensitivity and energy expenditure.15, 16 In addition, transplantation of white adipose tissue from these mice into the wild-type strain confers the enhanced metabolic profile observed in the DGAT-1 knockout mice. These studies have spurred research efforts to determine whether selective, small molecule inhibitors of DGAT-1 can produce the same improved metabolic profile observed in the DGAT-1−/− animals.