leaf extract inhibits Alzheimer's-like pathology through suppression of neuroinflammation.

Neuroinflammation is a crucial pathogenic process involved in the development and deterioration of Alzheimer's disease (AD). is known for its beneficial effects on various disease states such as allergic reaction, oxidative stress and inflammation. However, it is still unknown whether has protective effects on neuroinflammation, especially microgliosis related to AD. The current study aimed to investigate whether an extract of (named KP-1) protects from microglial cell activation and . To demonstrate the anti-neuroinflammation effects of KP-1, the current study adopted the most widely used experimental models including the lipopolysaccharide (LPS)-induced microgliosis model and amyloid beta (Aβ) oligomer (AβO)-induced neuroinflammation model, respectively. As a result, KP-1 pre-treatment reduced nitric oxide (NO) production, protein levels of inducible NO synthase (iNOS) and c-Jun N-terminal kinase (JNK) phosphorylation in BV2 cells which were significantly promoted by 100 ng ml LPS treatment. Similarly, KP-1 administration protected mice from AβO-induced memory impairment scored by Y-maze and novel object recognition test (NORT). Moreover, KP-1 administration suppressed AβO-induced microglial cell activation measured by counting the number of ionized calcium binding adaptor molecule 1 (Iba-1)-positive cells in both the cortex and hippocampal dentate gyrus and measuring the mRNA expression of TNFα, IL-1β and IL-6. Furthermore, AβO-induced synaptotoxicity was prevented by KP-1 administration which is in line with behavioral changes. Collectively, these findings suggest that KP-1 could be a potential functional food for protection against neuroinflammation, and prevents or delays the progression of AD.