OBJECTIVE: The objective of this study was to develop an ultrasound-assisted extraction (UAE) method for achieving a high extraction yield of anthraquinones using the response surface methodology (RSM), Box-Behnken design (BBD), and a recycling preparative high-performance liquid chromatography (HPLC) protocol for isolation of anthraquinones from C. singueana.
METHODOLOGY: Optimisation of UAE was performed using the Box-Behnken experimental design. Recycling preparative HPLC was employed to isolate anthraquinones from the root extract of C. singueana.
RESULTS: The BBD was well-described by a quadratic polynomial model (R2 = 0.9751). The predicted optimal UAE conditions for a high extraction yield were obtained at: extraction time 25.00 min, temperature 50°C and solvent-sample ratio of 10 mL/g. Under the predicted conditions, the experimental value (1.65 ± 0.07%) closely agreed to the predicted yield (1.64%). The obtained crude extract of C. singueana root was subsequently purified to afford eight anthraquinones.
CONCLUSION: The extraction protocol described here is suitable for large-scale extraction of anthraquinones from plant extracts.
DESCRIPTION: The hemibiotroph G. boninense establishes via root contact during early stage of colonization and subsequently kills the host tissue as the disease progresses. Information on the pathogenicity factors/genes that causes BSR remain poorly understood. In addition, the molecular expressions corresponding to G. boninense growth and pathogenicity are not reported. Here, six transcriptome datasets of G. boninense from two contrasting conditions (three biological replicates per condition) are presented. The first datasets, collected from a 7-day-old axenic condition provide an insight onto genes responsible for sustenance, growth and development of G. boninense while datasets of the infecting G. boninense collected from oil palm-G. boninense pathosystem (in planta condition) at 1 month post-inoculation offer a comprehensive avenue to understand G. boninense pathogenesis and infection especially in regard to molecular mechanisms and pathways. Raw sequences deposited in Sequence Read Archive (SRA) are available at NCBI SRA portal with PRJNA514399, bioproject ID.
AIM OF THE STUDY: In this context, supported with previous preliminary data of its antiplasmodial activity, this study was undertaken to determine the in vitro antiplasmodial and cytotoxicity activities of G. lanceolatus crude extracts and its major compounds.
MATERIALS AND METHODS: The in vitro antiplasmodial activity was determined by parasite lactate dehydrogenase (pLDH) assay on chloroquine-sensitive (3D7) and chloroquine-resistant (K1) strains of Plasmodium falciparum. The cytotoxicity activity was evaluated using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay on hepatocellular carcinoma (HepG2) and normal liver (WRL-68) cell lines.
RESULTS: The root methanol extract possessed potent antiplasmodial activity against both P. falciparum 3D7 and K1 strains (IC50 = 2.7 μg/ml, SI = 140; IC50 = 1.7 μg/ml, SI = 236). Apart from the DCM extract of stem bark and root that were found to be inactive (IC50 > 50 μg/ml) against 3D7 strain, all other tested crude extracts exhibited promising (5< IC50 30 µg/ml, CC50 > 10 µM, respectively), except for the hexane and DCM extracts of root, which exerted mild cytotoxicity on HepG2 cell line (IC50 plant extract. It is also noteworthy, that the extract and compound were more active against chloroquine-resistant (K1) strain of P. falciparum. Further studies are being carried out to assess their toxicity profile and antimalarial efficacy in animal model.
METHODS AND RESULTS: Here, we showed that three di-O-caffeoylquinic acids suppressed hepatic glucose production in H4IIE rat hepatoma cells by reducing expression of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK), two key enzymes that regulate hepatic gluconeogenesis. Direct comparisons between CQAs and their metabolites (3-caffeoylquinic, caffeic, and quinic acids) revealed the caffeic acid moiety alone was responsible for the observed effects. Further analysis suggested the activation of PI3K and MAPK pathways as a method of controlling gene expression was shared between caffeoylquinic and caffeic acids. These compounds promoted increased mitochondrial respiration and cellular metabolism, in part by inducing oxidative phosphorylation and proton leak.
CONCLUSION: We concluded that the caffeic acid moiety was important for suppression of hepatic gluconeogenesis and hyperglycemia, ultimately strengthening the link between dietary interventions based on caffeic acid-containing plant foods and healthy glucose metabolism.