(P27-019-23) Cordycepin, an Active Component of the Fungus Cordyceps militaris, Inhibits the Inflammatory Response of Rat Brain Microglial Cells Through MAPKs Pathway

Objectives: Microglia are the prime immune cells responsible for mediating immune and inflammatory responses within the central nervous system (CNS). Under abnormal conditions, the activation of microglia contributes to the restoration of normal functioning within the CNS. Nevertheless, prolonged activation of microglia can pose a threat to the survival of neurons due to the secretion of multiple inflammatory and neurotoxic molecules. Therefore, researchers have explored the possibility of utilizing inhibitors of microglial activation as a potential therapy to combat neurodegenerative conditions such as Alzheimer's and Parkinson's diseases. Cordycepin, a derivative of the nucleoside adenosine, is one of the active components extracted from fungi of genus Cordyceps, and has been shown to have many pharmacological activities in traditional oriental medicine. The specific aim of this study was to examine whether cordycepin represses microglial activation.

Methods: Primary microglial cells were prepared from cerebral cortices of one-day-old rat pups. And then confirm the isolation of microglia through the expression of CD11a/b and Iba1, which are markers of primary microglia, to confirm the effect of cordycepin on the LPS-induced inflammatory response after culture.

Results: As a result, nitric oxide (NO) increased due to LPS treatment, IL-1β, IL-6, and most of TNF-α were significantly reduced by cordycepin pretreatment. Treatment of primary microglia with cordycepin induced phosphorylations of p38 and ERK MAP kinase. Taken together, our results indicate that exposure to cordycepin exhibits anti-inflammatory activity in microgila cells through activation of the MARKs signaling pathway.

Conclusions: These results suggest that cordycepin may play an important role in neuropathological conditions by inducing various proinflammatory and neurotoxic molecules within microglia.

Funding Sources: Ministry of Science and ICT and the National Research Foundation of Korea