α-Phellandrene (α-PA) is a cyclic monoterpene. To investigate the induction of autophagy by α-PA and its mechanism, human liver tumor cells (J5) were incubated with α-PA and analyzed for cell viability and the molecular regulation of pre-autophagosome origination and autophagosome formation. According to the results, PI3K-I, mTOR, and Akt protein levels were decreased after α-PA treatment compared to those of the control group (p < 0.05). The phosphorylation of Bcl-2, and PI3K-III, LC3-II and Beclin-1 protein levels in J5 cells were increased after α-PA treatment (p < 0.05). In addition, α-PA up-regulated nuclear p53 and down-regulated cytoplasmic p53 expression in J5 cells. The NF-κB pathway was activated, as indicated by increase in cytosolic phosphorylated IκB, nuclear NF-κB levels, and the DNA-binding activity of NF-κB after α-PA treatment in J5 cells (p < 0.05). These results suggest that α-PA can induce J5 cell autophagy by regulating mTOR and LC-3II expression, p53 signaling, and NF-κB activation in J5 cells.

α-Phellandrene (α-PA) is a component of dietary spices and herbs. The effect of α-PA on anticancer is unclear. This study aims to investigate the effects of α-PA on liver tumor cell death fate. Human liver tumor (J5) cells were incubated with α-PA and analyzed for cell cycle distribution, expression of Bax, Bcl-2, poly (ADP-ribose) polymerase (PARP) protein, and caspase-3 activity of J5 cells, and levels of nitric oxide (NO) production, lactate dehydrogenase (LDH) leakage, and ATP depletion were also analyzed in this study. Results found that α-PA significantly (P < 0.05) decreased the cell viability of J5 cells after 24-h treatment. The cell cycle distribution, Bax, Bcl-2, PARP protein levels, and caspase-3 activity of J5 cells did not change for 24 h after treatment with 30 μM α-PA. Reactive oxygen species levels significantly increased, mitochondrial membrane potential levels significantly decreased when J5 cells were treated with 30 μM α-PA for 24 h (P < 0.05). Thirty μM α-PA significantly (P < 0.05) increased the necrotic cell number, NO production, LDH leakage, and ATP depletion after 24 h of incubation. These results suggest that α-PA induced J5 cell necrosis but not apoptosis, and α-PA-induced necrosis possibly involved ATP depletion.

The antityrosinase and antimutation effects of longan leaves and its bioactive compounds was investigated. The water extracts of longan leaves (WLL) inhibited the mutagenicity of 2-aminoanthracene, an indirect mutagen, and 4-nitroquinoline-N-oxide, a direct oxidative mutagen toward Salmonella typhimurium TA 98 and TA 100. WLL at 0-0.6 mg/ml displayed free radical scavenging activity, reducing power, chelating ability and protection against lipid oxidative damage. In addition, the inhibitory actions of WLL on tyrosinase activity and nitric oxide (NO) production in lipopolysaccharide (LPS) stimulated macrophages RAW 264.7 cell increased in concentration-dependent manner. According to HPLC-DAD analysis showed that epicatechin, ellagic acid and gallic acid, the major phenolic compounds, were present in WLL. The phenolic components may in part account for contributing the protective effects of WLL. On the basis of the results obtained, WLL can display biological functions and effectively protective against oxidation, mutation, tyrosinase, and inflammation.