Anti-cancer and antioxidant properties of phenolics isolated from Toona sinensis A Juss acetone leaf extract

Purpose: To investigate the antioxidant and anticancer activities of phenolics from the leaf extract of Toona sinensis (TS). Methods: Acetone leaf extract of TS was screened for total phenolic and flavanoid contents, and the flanonoids were subjected to high performance liquid chromatographic (HPLC) analysis. Antioxidant properties were assessed via oxygen radical absorbance capacity (ORAC), peroxyl radical scavenging capacity (PSC) and cellular antioxidant activity (CAA), while anti-proliferative activity ins HepG2 cell line was assessed using methylene blue assay. Results: The extract contained 36.02 ± 0.24 mg of gallic acid equiv/g dry weight (DW) and 20.24 ± 1.73 mg of catechin equiv/g DW of total phenolic and total flavonoid, respectively. The levels of rutin and quercitrin were 0.51 and 19.55 mg/g, respectively. Epicatechin, gallic acid, quercitin, isoquercetin were not detected. The extract showed significant antioxidant potential and high anti-proliferation capacity with low cytotoxicity against HepG2 cell in vitro. The underlying mechanism of anti-proliferative effect was induction of apoptosis. Conclusion: TS leaf extract possesses significant in vitro antioxidant properties and anti-proliferative effect against HepG2 cells, which make it a potential anticancer drug source.

Antitumor activity of physcion 8-o-β-glucopyranoside against cervical cancer by induction of apoptosis

Purpose: To investigate the antitumor activity of physcion8-O-β-glucopyranoside (PSG) against cervical cancer, as well as its mechanisms. Methods: The anti-proliferative effects of PSG on HeLa cells were determined by CCK-8 assay and the half maximal inhibitory concentration (IC50) values were calculated. Subsequently, a mouse xenograft model of HeLa cell line was established to investigate the antitumor effect of PSG in vivo. Furthermore, cell apoptosis was investigated by fluorescence microscopy via DAPI staining, and other mechanisms were determined by Western blot assay. Results: In vitro, PSG exhibited significant anti-proliferative effect on HeLa cells (p <0.05) in concentration-and time-dependent manners, with an IC50 value of 41.34 μg/mL. In vivo, PSG also had significant anti-tumor activity in nude mouse xenograft model (p < 0.05), inhibiting tumor growth. Furthermore, the results showed that treatment with PSG (20, 40 and 60 μg/mL) for 24 h resulted in significantly increased apoptosis in HeLa cells (p < 0.05). Additionally, Western blot analysis revealed that after exposure to 20, 40 and 60 μg/mL of PSG for 24 h, protein expressions of C-caspase-3, Ccaspase-9 and Bax were markedly up-regulated (p < 0.05) while Bcl-2 was significantly down-regulated (p < 0.05). These results confirmed that PSG inhibited HeLa cell growth by inducing mitochondriamediated apoptosis via up-regulation of caspase-3 and caspase-9 and Bax, and down-regulation of Bcl2. Conclusion: The results demonstrate that PSG possesses notable anti-tumor activity against cervical cancer and that the mechanisms involve induction of apoptosis by mitochondria-mediated signaling pathway.

Inhibition of proliferation, migration and invasion of human non-small cell lung cancer cell line A549 by phlomisoside F from Phlomis younghusbandii Mukerjee

Purpose: To determine the effect of phlomisoside F (PMF) on the proliferation, migration and invasion of human non-small cell lung cancer cell line A549 and explore the possible mechanisms. Methods: The anti-proliferative effect of PMF on A549 cells was determined by CCK-8. Subsequently, migration and invasion were evaluated by Transwell and Transwell with matrigel assays, respectively. Furthermore, cell cycle and apoptosis were assessed by flow cytometry, while the mechanisms of action were determined by Western blotting. Results: PMF exhibited significant anti-proliferative effect on A549 cells in concentration-dependent and time-dependent manners, with half maximal inhibitory concentration (IC50) of 54.51 μM. Treatment with PMF (10, 20 and 40 μM) for 48 h resulted in significantly decreased migration and invasion in A549 cells. In addition, PMF at concentrations of 25, 50 and 75 μM induced cell cycle arrest in G0/G1phase and enhanced cell apoptosis in A549 cells. Furthermore, caspase-3, caspase-9 and Bax protein expressions were up-regulated while Bacl-2 and COX-2 protein expressions were significantly downregulated at 10, 20 and 40 μM concentrations of PMF. Conclusion: PMF suppresses A549 cell growth, migration and invasion. The mechanism may be related to the induction of mitochondria-mediated apoptosis pathway via regulation of caspase-3, caspase-9, Bcl-2 and Bax expressions, and inhibition of PGE2 synthesis by reducing COX-2 expression.