Byrsonima sericea Ethanol Extract Protected PC12 Cells from the Oxidative Stress and Apoptosis Induced by 6-Hydroxydopamine.

Parkinson's disease is characterized by the progressive loss of dopaminergic neurons in the nigrostriatal pathway and oxidative stress is one of the main mechanisms that lead to neuronal death in this disease. Previous studies have shown antioxidant activity from the leaves of Byrsonima sericea, a plant of the Malpighiaceae family. This study aimed to evaluate the cytoprotective activity of the B. sericea ethanolic extract (BSEE) against the cytotoxicity induced by 6-hydroxydopamine (6-OHDA) in PC12 cells, an in vitro model of parkinsonism. The identification of phenolic compounds in the extract by HPLC-DAD revealed the presence of geraniin, rutin, isoquercetin, kaempferol 3-O-ß-rutinoside, and quercetin. The BSEE (75-300 µg/mL) protected PC12 cells from toxicity induced by 6-OHDA (25 µg/mL), protected cell membrane integrity and showed antioxidant activity. BSEE was able to decrease nitrite levels, glutathione depletion, and protect cells from 6-OHDA-induced apoptosis. Thus, we suggest that the BSEE can be explored as a possible cytoprotective agent for Parkinson's disease due to its high antioxidant capacity and anti-apoptotic action.

Effect of Byrsonima sericea DC. leaf extracts on mice gastrointestinal tract.

Byrsonima sericea DC. (Malpighiaceae) leaves are popularly folk medicine in Brazil used to treat gastro-intestinal disorders including diarrhea and gastric diseases. Ethanol extract (BSEE), ethyl acetate extract (BSEAE) and hexane extract (BSHE) of the leaf part of Byrsonima sericea DC were characterized for their total phenolics, proanthocyanidins and flavonoids content. The total antioxidant capacity of extracts was determined. The ethnopharmacological use of B. sericea leaves was evaluated by assaying BSEE for gastroprotective activity in stomach ulcer induced by indomethacin, intestinal motility and toxicity. Abundance of phenols mainly tannins was found in BSEE. Total phenolics, flavonoids and proanthocyanidins content in BSEE were found to be 0.371, 0.172 and 1.3 × 10-4 (mg/g) respectively. BSEE showed concentration dependent significant scavenging of DPPH values 90.0 (%) respectively. Moreover, oral doses of 500 and 1000 mg/kg did not cause mortality, and there was no difference in animals weight, organs relative weight and alanine transaminase (ALT) and aspartate transaminase (AST), as compared to the control group. Doses of 250, 500 and 1000 mg/kg inhibited the gastric lesions induced by indomethacin in 52, 60 and 62 % respectively. The dose of 1000 mg/kg decreased intestinal motility in animals. The presence of phenolic compounds, including tannins could be associated with the anti-diarrheal action and the antioxidant properties could collaborate to the gastroprotective and anti- diarrheal activities, confirming its popular use of the plant.

Caffeic acid protects mice from memory deficits induced by focal cerebral ischemia.

Brain ischemia pathophysiology involves a complex cascade of events such as inflammation and oxidative stress that lead to neuronal loss and cognitive deficits. Caffeic acid (CA) is a natural phenolic compound with antioxidant and anti-inflammatory properties. To evaluate the neuroprotective efficacy of this compound in mice subjected to a permanent middle cerebral artery occlusion, animals were pretreated and post-treated with CA, 2, 20, and 60 mg/kg/day, intraperitoneally, at 24, 48, 72, 96, or 120 h after ischemia. Animals were evaluated at 24 h after the permanent middle cerebral artery occlusion for brain infarction and neurological deficit score. At 72 h after the occlusion, animals were evaluated for locomotor activity, working memory, and short-term aversive memory; long-term aversive memory was evaluated 24 h after the evaluation of short-term aversive memory. Finally, at 120 h after the event, spatial memory and the expression levels of synaptophysin (SYP), SNAP-25, and caspase 3 were evaluated. The treatment with CA reduced the infarcted area and improved neurological deficit scores. There was no difference in locomotor activity between groups. The working, spatial, and long-term aversive memory deficits improved with CA. Furthermore, western blotting data showed that the expression of SYP, which correlates with synaptic formation and function, decreased after ischemic insult, and CA inhibited the reduction of SYP expression. Ischemia also increased, and CA treatment decreased, caspase 3 expression. These results suggest that CA exerts neuroprotective and antidementia effects, at least in part, by preventing the loss of neural cells and synapses in ischemic brain injury.