Neuroprotective effect of tormentic acid against memory impairment and neuro‑inflammation in an Alzheimer's disease mouse model.

Abstract

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.