Proposal for the classification of sinomenine alkaloids.

The chemical structure of sinoacutine is formed by a phenanthrene nucleus and an ethylamine bridge. Because it has a similar parent structure to morphine, it is subdivided into morphinane. At present, all reports have pointed out that the basic skeleton of morphine alkaloids is salutaridine (the isomer of sinoacutine), which is generated by the phenol coupling reaction of (R)-reticuline. This study shows that the biosynthetic precursors of sinoacutine and salutaridine are different. In this paper, the sinoacutine synthetase (SinSyn) gene was cloned from Sinomenium acutum and expressed SinSyn protein. Sinoacutine was produced by SinSyn catalyzed (S)-reticuline, according to the results of enzyme-catalyzed experiments. The optical activity, nuclear magnetic resonance, and mass spectrum of sinoacutine and salutaridine were analyzed. The classification and pharmacological action of isoquinoline alkaloids were discussed. It was suggested that sinoacutine should be separated from morphinane and classified as sinomenine alkaloids.

5-Caffeoylquinic acid decreases diet-induced obesity in rats by modulating PPARα and LXRα transcription.

BACKGROUND: Chlorogenic acids (CGAs) are widely distributed in plant material, including foods and beverages. 5-Caffeoylquinic acid (5-CQA) is the most studied CGA, but the mechanism of its hypolipidaemic effect remains unclear. This study aimed to determine the effect of 5-CQA on lipid metabolism in the liver of Sprague-Dawley rats fed a high-fat diet (HFD). RESULTS: 5-CQA suppressed HFD-induced increases in body weight and visceral fat-pad weight, serum lipid levels, and serum and hepatic free fatty acids in a dose-dependent manner. Real-time polymerase chain reaction revealed that 5-CQA altered the mRNA expression of the transcription factors peroxisome proliferator-activated receptor α (PPARα) and liver X receptor α (LXRα) and target genes involved in hepatic fatty acid uptake, ß-oxidation, fatty acid synthesis, and cholesterol synthesis. Moreover, hepatic tissue sections from HFD-fed rats showed many empty vacuoles, suggesting that liver cells were filled with more fat droplets. However, 5-CQA significantly ameliorated this effect. CONCLUSION: 5-CQA may improve lipid metabolism disorders by altering the expression of PPARα and LXRα, which are involved in multiple intracellular signalling pathways.