Piceatannol

Corinthian currant, a typical Mediterranean dried vine fruit, contains various bioactive phenolic compounds. The present study investigates the phytochemical composition of Corinthian currant through suspect screening of phenolic acids, flavonoids, and other phenolics. Using advanced mass spectrometry equipment, that is, the Exactive Plus Orbitrap and QToF, we developed and applied a methodology to identify 43 bioactive compounds, not previously reported as Corinthian currant constituents. For our study, samples from six distinct Greek cultivation areas were obtained; all 43 phenolics were present in all samples assessed. In terms of quantification, a semi-quantitative approach was applied; petunidin 3-O-arabinoside (2.18 ± 1.01 mg/100 g), peonidin 3-O-(6″-p-coumaroyl-glucoside (1.06 ± 0.81 mg/100 g), fertaric acid (1.16 ± 0.47 mg/100 g), isorhamnetin 3-O-glucoside (0.28 ± 0.10 mg/100 g), and piceatannol (0.23 ± 0.12 mg/100 g) predominated in Corinthian currants across all cultivation regions. Our findings reveal the rich and diverse phenolic profile of Corinthian currant, offering valuable insights into its potential health benefits.

Exposure to chronic unpredictable stress (CUS) serves as the major contributor for the neurobehavioral changes. The current study explores the possible involvement of the SIRT1 pathway in mediating the neuroprotective properties of piceatannol in CUS induced neurobehavioral changes. Molecular docking studies showed binding interactions of piceatannol with SIRT1, suggesting that it may modulate SIRT1 activity. For evaluating effect of CUS and pharmacological interventions on neurobehavioral changes, the mice (Swiss Albino, Male) were subjected to the EPM, TST, FST, SPT, MWM and PA test. In current study, the effect on levels of corticosterone and neurotransmitters (dopamine and serotonin); various parameters of oxidative stress and neuroinflammation; acetylcholinesterase and histological changes in hippocampus and cortex were also assessed. It was observed that piceatannol (10 and 20 mg/kg; p.o) reduced the deleterious impact of CUS on oxidative stress and neuroinflammation; reduced corticosterone and dopamine levels; increased serotonin levels and improved neurobehavioral and histological changes. Pre-treatment with sirtinol (10 mg/kg; i.p.), a SIRT1 inhibitor, greatly reduced the neuroprotective properties of piceatannol. Thus, it may be concluded that activation of SIRT1 pathway may be responsible for the neuroprotective effects of piceatannol on CUS induced neurobehavioral alterations.