Cognitive impairment and neuro‑inflammatory responses are the distinctive characteristics of Alzheimer's disease (AD). Tormentic acid (TA) is one of the major active components of Potentilla chinensis and has been demonstrated to have anti‑inflammatory properties. However, the potential effects of TA on neuro‑inflammatory responses and memory impairment in AD remain unknown. The present study investigated the therapeutic effect of TA on neuro‑inflammation, as well as learning and memory impairment in AD mice. In addition, the effects of TA treatment were also examined in a co‑culture system of microglia and primary neurons. Intraperitoneal administration of TA attenuated memory deficits in amyloid β precursor protein/presenilin 1 transgenic mice, with a marked decrease in amyloid plaque deposition. TA also reduced microglial activation and decreased the secretion of pro‑inflammatory factors in AD mice. Furthermore, pre‑treatment with TA suppressed the production of pro‑inflammatory markers, as well as the nuclear translocation of nuclear factor‑κB (NF‑κB) p65 induced by Aβ exposure in BV2 cells. TA also reduced inhibited neurotoxicity and improved neuron survival in a neuron‑microglia co‑culture system. Taken together, these findings suggested that TA could attenuate neuro‑inflammation and memory impairment, which may be closely associated with regulation of the NF‑κB pathway.
Keywords: alzheimer's disease; tormentic acid; nuclear factor-κB; inflammation; microglia.