Notopterygium incisum roots extract (NRE) alleviates neuroinflammation pathology in Alzheimer's disease through TLR4-NF-κB pathway.

Ethnopharmacological Relevance: Notopterygium incisum Ting ex H. T. Chang, also called 'Qianghuo', is a distinct umbelliferae plant in China. The rhizomes and roots of Notopterygium incisum have long been used to treat headaches, colds, analgesia and rheumatoid arthritis. It is a main traditional Chinese medicine in Qianghuo Yufeng Decoction, which was used to treat diseases such as liver and kidney insufficiency, mental paralysis and dementia.

Aim Of This Study: As the most common dementia, Alzheimer's disease (AD) has a complicated pathogenesis. So far, there is no effective drug to prevent its pathological process. Previous research has shown that Notopterygium incisum root extract (NRE) may inhibit the release of Aβ and the activation of tau in mice with AD. However, the effect of NRE on the pathological process of neuroinflammation is still unclear.

Materials And Methods: We determined the pro-inflammatory cytokines levels in BV2 cells exposed to LPS/Aβ42 after treated with NRE. APP/PS1 and LPS-induced C57BL/6 neuroinflammatory mice were given NRE for 8 weeks and 5 days respectively to detect the pathological changes of neuroinflammation.

Results: The findings showed that NRE had a notable inhibitory effect on the levels of TNF-α and IL-1β in BV2 cells induced by LPS/Aβ42. The results of in vivo experiments show that following NRE treatment, there was a notable decrease in the number of activated microglia in the hippocampus of APP/PS1 mice as indicated by immunofluorescence results. Sholl analysis showed that microglia branches increased in NRE group, indicating that M1 microglia activation was inhibited. In the mice model injected with LPS in the tail vein, PCR and Western Blot results confirmed the anti-inflammatory effect of NRE, Nissl staining showed the protective effect of NRE on neurons, and immunofluorescence results also indicated that the activation of M1 microglia was inhibited.

Conclusion: These results suggest that long term oral administration of NRE may inhibit neuroinflammation in the progression of AD.