Melatonin treatment maintains the quality and delays senescence of postharvest cattails (Typha latifolia L.) during cold storage

Melatonin treatment was investigated for the sensory quality and senescence in postharvest cattails (Typha latifolia L.) during cold storage. The 0.75 mM melatonin treatment reduced surface browning and delaying lignification of Cattails stored at 4 °C. The results showed that melatonin treatment slowed weight loss and firmness, maintained sensory quality and reducing sugar content. Melatonin treatment reduced browning by inhibiting the increase of MDA and H2O2 contents and POD activity. Melatonin treatment maintained high non-enzymatic antioxidant components (Vitamin C and total phenolic content) and antioxidant enzyme activities (SOD, CAT, and APX), thereby alleviating the browning and senescence of postharvest cattails. These findings indicate that melatonin treatment can maintain postharvest cattails quality

MSA enhances paclitaxel efficacy in vivo.

<p>(<b>A</b>) Tumor growth curve. Data are presented as tumor volumes in each group (n = 6 tumors/group). (<b>B</b>) Average tumor weight in each group at the end of the experiment. (<b>C</b>) Average body weight of the mice in each group. Error bars, SEM. *, statistically significant (<i>P</i><0.05) from the control group. **, statistically significant (<i>P</i><0.05) from both single-agent-treated sample and the control sample. Pac, paclitaxel.</p

MSA enhances the effect of paclitaxel in inhibiting cell proliferation and inducing apoptosis in MDA-MB-157 and BT-549 cells.

<p>Cells were treated with MSA, paclitaxel, or the combination for 48 hr, and then subjected to analysis for proliferation (<b>A, B</b>) or apoptosis (<b>C, D</b>). The BrdU and apoptosis readings were normalized by the SRB reading in cells set up in parallel. Error bars, SEM. *, statistically significant (<i>P</i><0.05) from the control group. **, statistically significant (<i>P</i><0.05) from both single-agent-treated sample and the control sample. Pac, paclitaxel.</p

Effect of MSA and/or paclitaxel on cell viability^*.

*<p><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031539#s3" target="_blank">Results</a> are expressed as % of vehicle control (mean ± SEM).</p

Inhibiting caspase activity attenuates apoptosis induction and growth suppression by MSA and paclitaxel in MDA-MB-231 cells.

<p>Cells were pre-treated with 50 µM pan-caspase inhibitor Z-VAD-FMK prior to treatment with 3.2 µM MSA, 10 nM paclitaxel, or the combination. Apoptosis was determined at the 16-hr time point by Cell Death ELISA (<b>A</b>), and cell viability at 72 hr by SRB (<b>B</b>). Error bars, SEM. *, statistically significant (<i>P</i><0.05) from the corresponding control sample not treated with the caspase inhibitor. Pac, paclitaxel.</p

MSA enhances the efficacy of paclitaxel in inhibiting the growth of MDA-MB-231 cells.

<p>Cells were treated with 3.2 or 4 µM MSA, 10 nM paclitaxel, or the combinations for 72 hr. Live cells were counted with trypan blue staining.</p

Effect of MSA and/or paclitaxel on cell cycle distribution^#.

#<p><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031539#s3" target="_blank">Results</a> are expressed as mean % of cells in a specific phase of cell cycle ± SEM.</p>*<p>Significantly different compared to the control group (<i>P</i><0.05).</p>**<p>Significantly different compared to both single-agent-treated and control groups (<i>P</i><0.05).</p

Induction of apoptosis and inhibition of tumor proliferation by paclitaxel and MSA in MDA-MB-231 xenograft.

<p>(<b>A</b>) TUNEL staining. Data are presented as mean number of TUNEL-positive cells in each image. (<b>B</b>) Ki-67 IHC. Data are presented as mean % of Ki-67-positive cells. Error bars, SEM. *, statistically significant (<i>P</i><0.05) from both single-agent-treated sample and the control sample. Pac, paclitaxel. Right panels: Representative images from each group.</p

20(S)-protopanaxadiol inhibition of progression and growth of castration-resistant prostate cancer.

Castration-resistant progression of prostate cancer after androgen deprivation therapies remains the most critical challenge in the clinical management of prostate cancer. Resurgent androgen receptor (AR) activity is an established driver of castration-resistant progression, and upregulation of the full-length AR (AR-FL) and constitutively-active AR splice variants (AR-Vs) has been implicated to contribute to the resurgent AR activity. We reported previously that ginsenoside 20(S)-protopanaxadiol-aglycone (PPD) can reduce the abundance of both AR-FL and AR-Vs. In the present study, we further showed that the effect of PPD on AR expression and target genes was independent of androgen. PPD treatment resulted in a suppression of ligand-independent AR transactivation. Moreover, PPD delayed castration-resistant regrowth of LNCaP xenograft tumors after androgen deprivation and inhibited the growth of castration-resistant 22Rv1 xenograft tumors with endogenous expression of AR-FL and AR-Vs. This was accompanied by a decline in serum prostate-specific antigen levels as well as a decrease in AR levels and mitoses in the tumors. Notably, the 22Rv1 xenograft tumors were resistant to growth inhibition by the next-generation anti-androgen enzalutamide. The present study represents the first to show the preclinical efficacy of PPD in inhibiting castration-resistant progression and growth of prostate cancer. The findings provide a rationale for further developing PPD or its analogues for prostate cancer therapy