FACS analysis showing distribution of cells % (cell cycle arrest at different phases).

<p>G2/M phase arrest was enhanced in PNKPi treated group comapred to control cells. **p<0.01; ***p<0.001, significance of difference compared to control and ^#p<0.05, ^##p<0.01 in comparison with the only irradiated group.</p

Bar graph represents the increase in absorbance (OD) at 405 nm due to the release of <i>p</i>-nitroanilide.

<p>Caspase-3 activity was highly increased in PNKPi treated group compare to only irradiated group.***p<0.001 significance of difference from only irradiated group.</p

Targeting DNA repair with PNKP inhibition sensitizes radioresistant prostate cancer cells to high LET radiation - Fig 4

<p><b>(A)</b> Morphological changes of PC-3 cells with and without PNKPi (A12B4C3) treatment after 2Gy and 4Gy of ¹²C beam. The combination treated group showedmorphological changes as compare to only irradiated and control cells. <b>(B)</b>Cellpopulation decreased in combination treatment samples.***p<0.001, significance of difference from control and ^#p<0.05in comparison with the only irradiated group.<b>(C)</b>Cell proliferaton (%) decreased when ¹²C beam is combined with PNKPi. ***p<0.001, significance of difference from control and ^###p<0.001, significance of difference from only irradiated group respectively.</p

Surviving fraction (SF) graphs of PC-3 cells.

<p>(<b>A)</b>Note a dose dependent SF curve when PC-3 cell were treated with ¹²C beam only. <b>(B)</b> Effect of different concentration of PNKPi A12B4C3 on SF of PC-3 cells note that cells were least toxic till 10μM concentration.<b>(C-F)</b> Effect of different doses of ¹²C beam (<b>―</b>)with different concentration of A12B4C3 (…..) note a decrease in the SF as the concentration of A12B4C3 increases with ¹²C irradiation.</p

Schematic work flow for experiments.

<p>Schematic work flow for experiments.</p

Development, characterization and toxicological evaluations of phospholipids complexes of curcumin for effective drug delivery in cancer chemotherapy

<p>The purpose of this study was to prepare and characterize the complexes between curcumin (CU) phosphatidylcholine (PC) and hydrogenated soya phosphatidylcholine (HSPC) and to evaluate their anticancer activity. These CU–PC and CU–HSPC complexes (CU–PC-C and CU–HSPC-C) were evaluated for various physical parameters like Fourier transform infrared spectroscopy, melting point, solubility, scanning electron microscopy and the <i>in vitro</i> drug release study. These data confirmed the formation of phospholipids complexes. The <i>in vitro</i> hemolysis study showed that the complex was non-hemolytic. The anti-cancer potential of the complexes was demonstrated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay in MCF-7 cell line. This increase may be due to the amphiphilic nature of the complexes, which significantly enhances the water and lipid solubility of the CU. Unlike the free CU (which showed a total of only 90% drug release at the end of 8 h), complex showed around 40–60% release at the end of 8 h in dissolution studies. It showed that (when given in equimolar doses) complexes have significantly decreased the amount of CU available for absorption as compared with CU-free drug. Both CU-PC-C and CU-HSPC-C were found to be non-toxic at the dose equivalent to 2000 mg/kg of body weight of CU in the toxicity study. Acute and subacute toxicity studies confirmed the oral safety of the formulation. A series of genotoxicity studies was conducted, which revealed the non-genotoxicity potential of the developed complexes. Thus, it can be concluded that the phospholipid complexes of CU may be a promising candidate in cancer therapy.</p