Aim To investigate the anti-inflammatory molecular mechanism of chlorogenic acid extracted from Lonicera confusa DC in vitro.Methods PM? of a rat was segregated.MTT assay was used to detect the effects of the chlorogenic acid on PM? cells growth activities. PM? was stimulated with LPS for a prolonged period,ELISA was used to detect the level of TNF-?,IL-6 and PGE2 in the supernatant;COX-2 activity was determined by the level of PGE2 in the supernatant.After stimulating PM? with A23187 for a short time,the 6-keto-PGF1? level in the supernatant was measured by radioimmunoassay to express COX-1 activity.Results Chlorogenic acid had no inhibitive effects between 31.25 mg?L-1 and 1000 mg?L-1.The level of TNF-?,IL-6 and PGE2 in drug groups was lower than that of LPS-induced group,and the difference was significant,in a dose-dependent manner.The concentration of 50 mg?L-1 group was ineffective in the expression of TNF-?.Low concentration chlorogenic acid inhibited the expression of 6-keto-PGF1?,while high-concentration induced it.Conclusions The anti-inflammatory effect of chlorogenic acid may be related to inhibiting TNF-?,IL-6 activity and affecting exogenous AA metabolism.

Alzheimer's disease （AD） is a chronic neurodegenerative disorder characterized by the progressive loss of cognitive and memory functions. Its pathological features mainly include neurofibrillary tangles formed by the aggregation of hyperphosphorylated tau proteins and amyloid plaques formed by the accumulation of β-amyloid. The exact pathogenesis of AD has not been fully elucidated， and there are currently no effective specific drugs or radical treatments available in clinical practice. In recent years， the incidence of AD has been on the rise， severely affecting life and health， making the search for effective drugs and therapeutic components for AD treatment crucial. Modern medical research has found that the brain-derived neurotrophic factor （BDNF）/tropomyosin receptor kinase B （TrkB） signaling pathway is closely related to neurogenesis， apoptosis， neuroinflammation， synaptic plasticity， and oxidative stress， playing a vital role in the pathophysiological development of AD. Additionally， Chinese medicine has a long history of treating neurodegenerative diseases with few adverse reactions and features a multi-target， multi-link， and multi-pathway approach to treatment. Therefore， the author reviewed the latest research reports in China and abroad to elaborate on the role of the BDNF/TrkB signaling pathway in the onset and progression of AD， and summarized the research progress on the regulation of the BDNF/TrkB pathway by Chinese medicine compounds and monomers in AD intervention. This study is expected to provide references for the development of clinical drugs for the prevention and treatment of AD and to broaden the perspective on Chinese medicine treatment of AD.