In vitro evaluation of anti-inflammatory, antioxidant, and anti-acetylcholinesterase activities of apple and date vinegar extracts added with centella asiatica / Nor Atiqah Jusril

Neuroinflammation and oxidative stress are major factors of neurodegenerative damage correlated to cognitive impairment in Alzheimer's disease (AD). It results primarily from overproduction of oxidative stress that induce activation of pro-inflammatory cytokines causing to neuronal death. This study investigated the anti-inflammatory, antioxidant, and anti-acetylcholinesterase activities of apple and date vinegar added with Centella asiatica in SH-SY5Y neuroblastoma cells. The neuroprotective effect of apple or date vinegar added with various percentage of C. asiatica (0, 0.5, 2, 5%) was determined in vitro. The methanolic extract of apple vinegar added with C. asiatica [AV-CA (2%)] and date vinegar added with C. asiatica [DV-CA (2%)] extracts showed potent neuroprotective effect. Both extracts were subjected to liquid-liquid partitioning yielded aqueous (H20: AV-CA/DV-CA) and ethyl acetate (EA: AV-CA/DV-CA) at [2% CA] extracts. All of extracts were tested for anti-inflammatory, antioxidant, and anti- acetylcholinesterase activities. Anti-inflammatory response against nitric oxide (NO) was measured in SH-SY5Y neuroblastoma cells. Meanwhile, the intercellular reactive oxygen species ROS inhibition was measured as antioxidant activity and percentage inhibition of acetylcholinesterase (AChE) was measured by using commercially available kit's test. In general, all extracts significantly (P < 0.05) inhibited NO production without affecting cell viability. EA-DVCA extract showed better NO production inhibition and induced more attenuation effect on nitrite production with an IC50 value of 563.5 ±0.13 ug/mL. Furthermore, EA: AV-CA extract showed a high percentage ROS inhibition with an IC50 value of 17.54 ± 0.40 ug/mL. Strongest AChE inhibition activity was observed in EA: DV-CA (2%) with (IC50 = 9.087 ug/mL. It is suggested that the ameliorating effect of EA: DV-CA (2%) on LPSinduced neuroinflammation and memory deficit seems to be attenuated via antiinflammatory, inhibition of reactive oxygen species and AChE activities.