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opennotspecifiedMar 2017View details →

Table 2 in Cytotoxicity of methanolic extract of Swertia petiolata against gastric cancer cell line SNU- 5 is via induction of apoptosis ⁎

<p><b>Table 2</b> LC–MS identification of major constituents of methanolic extract of <i>Swertia petiolata</i>. The retention time peak numbers are as per Fig. 6.</p><table><tbody><tr><th>Peak no.</th><th>Retention time (minutes)</th><th>M-H</th><th>M + H</th><th>Molecular weight</th><th>Compound</th></tr></tbody><tbody><tr><th>1</th><td>7.6</td><td>355</td><td>–</td><td>354</td><td>Chlorogenic acid</td></tr><tr><th>2</th><td>9.9</td><td>163</td><td>165</td><td>164</td><td><i>p</i> -Coumaric acid</td></tr><tr><th>3</th><td>11.2</td><td>–</td><td>455</td><td>456</td><td>Ursolic acid</td></tr><tr><th>4</th><td>12.4</td><td>–</td><td>465</td><td>464</td><td>Myrecetin 3- <i>O</i> -rahamnoside</td></tr><tr><th>5</th><td>15.1</td><td>326</td><td>–</td><td>327</td><td>Unidentified</td></tr><tr><th>6</th><td>15.9</td><td>433</td><td>435</td><td>434</td><td>Quercetin 3-arabinoside</td></tr><tr><th>7</th><td>18.5</td><td>447</td><td>–</td><td>448</td><td>Kaempherol 3- <i>O</i> -glucoside</td></tr><tr><th>8</th><td>21.3</td><td>271</td><td>273</td><td>272</td><td>Naringenin</td></tr><tr><th>9</th><td>22.4</td><td>269</td><td>–</td><td>270</td><td>Genistein</td></tr><tr><th>10</th><td>26.2</td><td>315</td><td>–</td><td>316</td><td>Isorhamnetin</td></tr><tr><th>11</th><td>28.7</td><td>287</td><td>289</td><td>288</td><td>Swerchirin</td></tr></tbody></table>

opennotspecifiedMar 2017View details →

Table 1 in Cytotoxicity of methanolic extract of Swertia petiolata against gastric cancer cell line SNU- 5 is via induction of apoptosis ⁎

<p><b>Table 1</b> IC 50 of methanolic extract of <i>S</i>. <i>petiolata</i> against different cancer cell lines determined by MTT assay.</p><table><tbody><tr><th>Cell line</th><th>IC50 (μg/ml)</th></tr></tbody><tbody><tr><th>Human lung cancer cell line A-549</th><td>75</td></tr><tr><th>Human prostate cancer cell line PC-3</th><td>125</td></tr><tr><th>Human breast cancer cell line MCF-7</th><td>75</td></tr><tr><th>Human gastric cancer cell line SNU-5</th><td>64</td></tr><tr><th>Human pancreas cancer cell line MiaPaca-2</th><td>75</td></tr><tr><th>Human normal cell line fR2</th><td>250</td></tr></tbody></table>

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Data from: Systems biology of tissue-specific response to Anaplasma phagocytophilum reveals differentiated apoptosis in the tick vector Ixodes scapularis

Anaplasma phagocytophilum is an emerging pathogen that causes human granulocytic anaplasmosis. Infection with this zoonotic pathogen affects cell function in both vertebrate host and the tick vector, Ixodes scapularis. Global tissue-specific response and apoptosis signaling pathways were characterized in I. scapularis nymphs and adult female midguts and salivary glands infected with A. phagocytophilum using a systems biology approach combining transcriptomics and proteomics. Apoptosis was selected for pathway-focused analysis due to its role in bacterial infection of tick cells. The results showed tissue-specific differences in tick response to infection and revealed differentiated regulation of apoptosis pathways. The impact of bacterial infection was more pronounced in tick nymphs and midguts than in salivary glands, probably reflecting bacterial developmental cycle. All apoptosis pathways described in other organisms were identified in I. scapularis, except for the absence of the Perforin ortholog. Functional characterization using RNA interference showed that Porin knockdown significantly increases tick colonization by A. phagocytophilum. Infection with A. phagocytophilum produced complex tissue-specific alterations in transcript and protein levels. In tick nymphs, the results suggested a possible effect of bacterial infection on the inhibition of tick immune response. In tick midguts, the results suggested that A. phagocytophilum infection inhibited cell apoptosis to facilitate and establish infection through up-regulation of the JAK/STAT pathway. Bacterial infection inhibited the intrinsic apoptosis pathway in tick salivary glands by down-regulating Porin expression that resulted in the inhibition of Cytochrome c release as the anti-apoptotic mechanism to facilitate bacterial infection. However, tick salivary glands may promote apoptosis to limit bacterial infection through induction of the extrinsic apoptosis pathway. These dynamic changes in response to A. phagocytophilum in I. scapularis tissue-specific transcriptome and proteome demonstrated the complexity of the tick response to infection and will contribute to characterize gene regulation in ticks.

opencc-zeroDec 2014View details →

Figure 5 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654

Figure 5 Compound 5 induces the ER-mediated apoptosis. A) Representative Western blot showing the enhanced release of Smac/DIABLO but not cytochrome c from the mitochondria (MF) into the cytosol (CF) of compound 5-treated A549 lung cancer cells (GI50). Equal protein loading was controlled by staining membranes with Ponceau S (a representative section of the stained membrane is shown). The experiment was repeated three times and the corresponding quantification is shown in (B), B) Quantification of smac/DIABLO and cytochrome C levels in vehicle-treated control A549 cells and cells treated with GI50 amount of compound 5 or 5% DMSO as a negative control. M: mitochondria fraction; C: cytosol fraction. Scale bars: mean ± SEM of three independent experiments. ** p < 0.01 compared to vehicle-treated control cells, C) Representative Western blot showing the induction of phosphorylation of eukaryotic initiation factor-2 (eIF-2) in A549 cells treated with GI50 amounts of compound 5. For comparison purposes, thapsigargin (TG), an ER stress-causing drug was used (3 μM, 2 h) as a positive control. The experiment was repeated three times.

Figure 4 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654

Figure 4 Compound 5 causes caspase activation. A) qRT-PCR analysis of caspase 3, 4, 8 and 9 mRNA in compound 5-treated cells (GI50) as compared to vehicle-treated control cells [set as 1 arbitrary unit (a.u.)]. Values were normalized to β-actin. Scale bars: mean ± SEM of three independent experiments performed in triplicates. *p < 0.05, **p < 0.01 compared to vehicle-treated control cells, B) Representative Western blots showing cleavage "activation' of procaspase 3 to the active form p17, procaspase 4 to the active form p20, and procaspase 9 to the active forms p35/p37. C: vehicle-treated control cells; 0.5%: 0.5% DMSO-treated cells; 1%: 1% DMSO-treated cells; 5%: 5% DMSO-treated cells; C.5: Compound 5-treated cells. The experiment was repeated three times.

Figure 2 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654

Figure 2 The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide) assay results for compound 5 against MCF10A cells, and white blood cells (WBC) after 24, 48 and 72 h of treatment.

Figure 3 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654

Figure 3 Compound 5 induces apoptosis in A549 lung cancer cells. A) Fluorescence images of A549 lung cancer cells showing fragmented nuclei after DAPI staining. Scale bar: 10 µm, B) Detection of DNA fragmentation by agarose gel electrophoresis. Cells were treated and genomic DNA was extracted and electrophoresed on 1.5% agarose gels. M: DNA molecular weight marker; C: vehicle-treated control cells; 1%: 1% DMSO-treated cells; 5%: 5% DMSO-treated cells; C.5: Compound 5-treated cells. Arrows indicate DNA fragments. Three experiments were performed with similar results.

Figure 6 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654

Figure 6 3D View of the target compounds (5, 7A, 6B and 6C) docked against ATP binding site of EGFR kinase.

opencc-by-4.0Feb 2023View details →

Raw Data for the article: Human Amnion-Derived Mesenchymal Stromal/Stem Cells Pre-Conditioning Inhibits Inflammation and Apoptosis of Immune and Parenchymal Cells in an In Vitro Model of Liver Ischemia/Reperfusion

<p>Ischemia/reperfusion injury (IRI) represents one of the leading causes of primary non-function acute liver transplantation failure. IRI, generated by an interruption of organ blood flow and the subsequent restoration upon transplant, i.e., reperfusion, generates the activation of an inflammatory cascade from the resident Kupffer cells, leading first to neutrophils recruitment and second to apoptosis of the parenchyma. Recently, human mesenchymal stromal/stem cells (hMSCs) and derivatives have been implemented for reducing the damage induced by IRI. Interestingly, sparse data in the literature have described the use of human amnion-derived MSCs (hAMSCs) and, more importantly, no evidence regarding hMSCs priming on liver IRI have been described yet. Thus, our study focused on the definition of an in vitro model of liver IRI to test the effect of primed hAMSCs to reduce IRI damage on immune and hepatic cells. We found that the IFNγ pre-treatment and 3D culture of hAMSCs strongly reduced inflammation induced by M1-differentiated macrophages. Furthermore, primed hAMSCs significantly inhibited parenchymal apoptosis at early timepoints of reperfusion by blocking the activation of caspase 3/7. All together, these data demonstrate that hAMSCs priming significantly overcomes IRI effects in vitro by engaging the possibility of defining the molecular pathways involved in this process.</p>

openodc-byJun 2023View details →

Supporting Data - Temperature and immunostimulants modulate transcription of the ubiquitin and apoptosis pathways in the Antarctic Harpagifer antarcticus and sub-Antarctic Harpagifer bispinis

<p>C<sub>t</sub> values obtained from Real-Time PCR (<em>ß-ACTIN</em>, <em>UBE3</em>, <em>SMAC/DIABLO</em> and <em>BAX</em> genes) of cDNA from liver, gills and spleen of <em>Harpagifer antarcticus</em> and <em>Harpagifer bispinis</em> fish stimulated with LPS, Poly I:C or non-stimulated (control, PBS-injected) under three temperatures (2, 5 and 8°C).</p>

Fig. 2. Key HMBC, 1H– 1H in Hyperelodiones A-C, monoterpenoid polyprenylated acylphoroglucinols from Hypericum elodeoides, induce cancer cells apoptosis by targeting RXRα

Fig. 2. Key HMBC, 1H– 1H COSY and NOESY correlations of compounds 1–3.

Fig. 4 in Hyperelodiones A-C, monoterpenoid polyprenylated acylphoroglucinols from Hypericum elodeoides, induce cancer cells apoptosis by targeting RXRα

Fig. 4. Experimental ECD spectra of 1–3.

Fig. 1 in Hyperelodiones A-C, monoterpenoid polyprenylated acylphoroglucinols from Hypericum elodeoides, induce cancer cells apoptosis by targeting RXRα

Fig. 1. Structure of compounds 1–3.

Fig. 3 in Hyperelodiones A-C, monoterpenoid polyprenylated acylphoroglucinols from Hypericum elodeoides, induce cancer cells apoptosis by targeting RXRα

Fig. 3. Calculated and experimental ECD spectra of 1 and two tautomers.

Fig. 2 in Diterpenoid alkaloids from Aconitum anthoroideum that offer protection against MPP -Induced apoptosis of SH-SY5Y cells and acetylcholinesterase inhibitory activity

Fig. 2. Plausible biosynthetic pathway of anthoroidine a (1).

Fig. 1 in Diterpenoid alkaloids from Aconitum anthoroideum that offer protection against MPP -Induced apoptosis of SH-SY5Y cells and acetylcholinesterase inhibitory activity

Fig. 1. Structures of compounds 1–24.

Fig. 5 in Diterpenoid alkaloids from Aconitum anthoroideum that offer protection against MPP -Induced apoptosis of SH-SY5Y cells and acetylcholinesterase inhibitory activity

Fig. 5. ORTEP drawing of 19.

Fig. 3 in Diterpenoid alkaloids from Aconitum anthoroideum that offer protection against MPP -Induced apoptosis of SH-SY5Y cells and acetylcholinesterase inhibitory activity

Fig. 3. Plausible biosynthetic pathway of anthoroidine B (2).

Fig. 4 in Diterpenoid alkaloids from Aconitum anthoroideum that offer protection against MPP -Induced apoptosis of SH-SY5Y cells and acetylcholinesterase inhibitory activity

Fig. 4. ORTEP drawing of 7.