Embelin induced changes in MAP kinase phosphorylation does not involve cross-talk between MAP kinases.

<p>A549 cells were pre-treated with or without U0126 (5 µM), PD169316 (5 µM), SP600125 (5 µM) for 1h followed by embelin (15 µM) for 4h. Total and phosphorylated levels of ERK 1/2, p38, JNK 1/2 and tubulin (loading control) were detected by Western blotting as described in the “Materials and Methods” section.</p

Effect of embelin and SMAC-N7-Ant peptide on cellular apoptosis.

<p>(<b>A</b>) A549 cells were treated with 15 µM embelin for different time intervals. Following the termination of treatments, caspase-3 activity was measured as indicated in the “Materials and Methods” section. (<b>B</b>) A549 cells were treated with 15 µM embelin for 4h and stained with Annexin-V/FITC and propidium iodide as described in the “Materials and Methods” section. Fluorescence images were captured using an Olympus–IX71 inverted fluorescence microscope equipped with FITC and rhodamine filter settings. Representative images from three different fields of view are shown. (<b>C</b>) Cells were treated with an XIAP inhibitor, SMAC-N7-Ant peptide (100 µM) for 8h. Later, caspase-3 and -9- activities were measured using the tetra-peptide substrates as described under “Materials and Methods” section. For both (<b>A</b>) and (<b>C</b>) data presented are the mean ± SD of three separate experiments. **indicates p<0.01 and * indicates p<0.05 as compared with controls.</p

Antioxidants abrogate embelin induced oxidative stress.

<p>(<b>A</b>) A549 cells were pretreated with or without FeTMPyP (10 µM) or NAC (10 mM) for 1h followed by embelin (15 µM) for 4h and ROS generation was detected by DCF staining as described in the “Materials and Methods” section. Cellular fluorescence was captured using an Olympus–IX71 inverted fluorescence microscope equipped with FITC filter settings. (<b>B</b>) Mean fluorescence intensity from three different fields of view were obtained using ImageJ software. * indicates p<0.05 as compared with control and # indicates p<0.05 as compared with embelin treated cells.</p

Embelin induced oxidative stress regulates MAPK mediated apoptosis.

<p>A549 cells were pre-treated with or without the antioxidant FeTMPyP (10 µM) for 1h followed by embelin (15 µM) treatment for 4h. (<b>A</b>) Cellular levels of total and phosphorylated ERK 1/2, p38, JNK 1/2 and tubulin were detected by Western blot followed by chemiluminescence detection as described under “Materials and Methods” section. (<b>B</b>) Under similar experimental conditions as (<b>A</b>), cellular caspase-3 activity was measured as described under “Materials and Methods” section. Data presented are the mean ± SD of three separate experiments. <b>*</b> indicates p<0.01 as compared to control and <b>#</b> indicates p<0.05 as compared to embelin treated cells.</p

Cytotoxicity of embelin in cancer and normal cell lines.

<p>(<b>A</b>) Structure of Embelin (<b>B</b>) Cells were treated with embelin for 48h and following the termination of incubation, cell viability was measured by sulphorhodamine B assay and IC₅₀ values were calculated as mentioned in the “Materials and Methods” section. Data shown are mean ± SD of three separate experiments. * indicates p<0.01as compared with controls.</p

Alterations in pathway based gene expression profile induced by embelin.

<p>A549 cells were treated with embelin (15 µM) for 4h. Microarray analysis was performed as described in “Materials and Methods” section. Genes that showed differential regulation by at least 2-fold with p<0.05 were classified based on functional category and pathways using GeneSpring GX and Genotypic Biointerpreter-Biological Analysis Software. Pathways that predominantly showed differential expression were (<b>A</b>) MAP Kinase pathway, (<b>B</b>) Cytokine-cytokine receptor interaction and (<b>C</b>) p53 pathway. The data has been submitted to GEO database with accession number GSE50545.</p

Asymmetric Total Synthesis of Stagonolide F

<div><p></p><p>A highly convergent stereoselective total synthesis of stagonolide F is described starting from commercially available 5-hexen 1-ol using asymmetric dihydroxylation, Jacobsen^'s hydrolytic kinetic resolution (HKR), regioselective epoxide ring opening with vinyl Grignard reaction, esterification, and ring-closing metathesis (RCM) as key steps.</p> </div

Advanced glycation end-products inhibitors isolated from <i>Schisandra grandiflora</i>

<div><p>Free radicals scavenging and advanced glycation end-products (AGEs) inhibitory potentials in crude chloroform extract of <i>Schisandra grandiflora</i> were evaluated. Bioassay-guided isolation of the chloroform extract led to the identification of 24 compounds. Among the isolates, ( ± ) gomisin M₁, arisantetralone C and D, macelignan, saurulignan B and SZ-MO displayed potent-free radical scavenging as well as AGEs inhibitory potentials. This is the first report identifying the presence of AGEs inhibitory activity and assigning AGEs inhibitory activity to these compounds. Therefore, our research finds new application of traditional medicinal plant <i>S. grandiflora</i> having capacity to reduce formation and accumulation of AGEs in diabetes.</p></div