Effects of ellagic acid on chemosensitivity to 5-fluorouracil in colorectal carcinoma cells.

Ellagic acid has been demonstrated to inhibit the growth of several types of cancer cells. However, whether it sensitizes human colorectal carcinoma cells to 5-fluorouracil, has not yet been investigated. Colorectal carcinoma HT-29, Colo 320DM, SW480 and LoVo cells were treated with ellagic acid (2.

Neuroprotective effects of carnosic acid on neuronal cells under ischemic and hypoxic stress.

Ischemia/hypoxia induces oxidative stress which is associated with neurodegenerative diseases. The present study investigated protective mechanism of carnosic acid (CA) on ischemia/reperfusion and hypoxia-induced neuronal cell injury. The results showed that CA reduced 52% of the infarct volume from brains under ischemia/reperfusion in vivo and protected the PC12 cells from hypoxic injury in vitro.

Rescue of p53 blockage by the A(2A) adenosine receptor via a novel interacting protein, translin-associated protein X.

Blockage of the p53 tumor suppressor has been found to impair nerve growth factor (NGF)-induced neurite outgrowth in PC-12 cells. We report herein that such impairment could be rescued by stimulation of the A(2A) adenosine receptor (A(2A)-R), a G protein-coupled receptor implicated in neuronal plasticity. The A(2A)-R-mediated rescue occurred in the presence of protein kinase C (PKC) inhibitors or protein kinase A (PKA) inhibitors and in a PKA-deficient PC-12 variant.

Regulation of type VI adenylyl cyclase by Snapin, a SNAP25-binding protein.

In the present study, we used the N terminus (amino acids 1 approximately 160) of type VI adenylyl cyclase (ACVI) as bait to screen a mouse brain cDNA library and identified Snapin as a novel ACVI-interacting molecule. Snapin is a binding protein of SNAP25, a component of the SNARE complex. Co-immunoprecipitation analyses confirmed the interaction between Snapin and full-length ACVI.