Antiproliferative and cytotoxic activity of extracts from Cistus incanus L. and Cistus monspeliensis L. on human prostate cell lines.

Benign prostatic hypertrophy (BPH) is a common condition in elderly men that impairs quality of life and leads to a number of medical complications. The use of phytotherapeutic compounds in patients with relatively moderate BPH symptoms has been growing steadily. In the present study, acute toxicity of lyophilised aqueous extracts of Cistus incanus L. and Cistus monspeliensis L., collected in Sicily, was evaluated on the shrimp (Artemia salina L.) lethality assay, an alternative test to determine the toxicity of natural products. The cytotoxic and growth inhibitory effects were studied on normal human prostate cells (PZ-HPV-7 and PNT1A) and on a lung fibroblast cell line (V79-4). Cell proliferation was evaluated by MTT and SRB assays. Cytotoxicity was measured using the Trypan blue exclusion assay. Cistus extract treatment on prostate cell lines resulted in an almost identical growth inhibitory response and in a significant decrease in an cell viability. These findings indicate the biologically relevant effect of polyphenolic compounds present in Cistus extracts, and suggest that these substances may prove beneficial in BPH treatment.

Trail interacts redundantly with nitric oxide in rat astrocytes: potential contribution to neurodegenerative processes.

The proapoptotic cytokine TRAIL has been shown to enhance amyloid-beta-dependent neurotoxicity. Here are reported interactions between TRAIL and nitric oxide (NO) in cultured rat astrocytes in vitro. Rat astrocytes expressed all TRAIL receptor mRNAs and proteins. However, TRAIL failed in inducing apoptosis of astrocytes, whereas these cells released substantial amounts of nitrites. A TRAIL-neutralizing antibody was able to prevent LPS-induced iNOS expression in astrocytes. Interestingly, TRAIL induced its own expression in astrocytes. These data suggest that redundancy between TRAIL and NO in astrocytes could be fueling neuronal damage/death processes, potentially uncovering novel molecular targets for the treatment of neurodegenerative disorders.