Experimental research is making considerable efforts to understand the rules that regulate the balance between toxic and protective brain innate immunity. Sigma-1 receptors are expressed in both neurons and glia are a unique class of intracellular proteins and is involved in neurodegeneration. (+)-Pentazocine is a known selective sigma-1 agonist. Our aim was to evaluate the biological effects of (+)-Pentazocine in microglia following hypoxia/reoxygenation condition. BV2 cells were exposed to 3 hours of hypoxia and 24h of reoxygenation. Cells were treated with sigma-1 agonist (+)-Pentazocine (1 μM, 10μM, 25μM and 50μM). We assessed cell viability, apoptosis, reactive oxygen species (ROS) formation, mitochondria membrane potential, and total thiol groups content (GSH). Our results showed that 24h of reoxygenation resulted in a significant decrease of cell viability and increase in apoptosis when compared to control. Cells treated by concentration of 25 μM of (+)-Pentaziocine shown viability like untreated cells. Furthermore, all treatments resulted in a significant decrease of ROS formation when compared to untreated cells. Finally, pharmacological treatments restored mitochondrial membrane potential when compared to the untreated group. Consistently with these results, we also showed that GSH content was restored following pharmacological treatments. The results showed that (+)- Pentazocine exhibit significant antioxidant activity and induce apoptosis in activated microglia, thus providing a new tool for effective manipulation of brain inflammation, with the specific aim of favoring its protective arm and boosting innate neuroprotective mechanisms.
|Titolo:||Antioxidant activity of (+)-Pentazocine on activated microglia|
MARRAZZO, Agostino (Corresponding)
|Data di pubblicazione:||2015|
|Appare nelle tipologie:||4.2 Abstract in Atti di convegno|