In this study, we investigated the effect of the extracts of Cyrtomium fortunei J.Sm. (CFJ) on lipopolysaccharide (LPS) induced inflammation in mouse BV-2 microglial cells. Nitric oxide (NO) production and cell viability were measured using the Griess reagent and the (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) (MTT) assay. Inflammatory cytokines were detected by quantitative polymerase chain reaction (qPCR) in BV-2 microglial cells with and without CFJ extracts. Subsequently, mitogen-activated protein kinases (MAPKs) and antioxidant markers were assessed by western blot analysis. It was found that the CFJ extract significantly decreased the production of pro-inflammatory cytokines (interleukin [IL]-6, tumor necrosis factor [TNF]-, and IL-1) and NO in BV-2 microglial cells that were stimulated with LPS. In addition, the expression levels of the phosphorylation of the MAPK family (p38, c-Jun N-terminal kinases [JNK], and extracellularsignal regulated kinase [ERK]) were reduced by CFJ. Also, treatment with CFJ significantly increased the activities of superoxide dismutase type 1(SOD1) and Catalase in BV-2 microglial cells. Our results indicate that CFJ has a potent suppressive effect on the pro-inflammatory responses of activated BV-2 microglia. Therefore, CFJ has the potential to be an effective treatment for neurodegenerative diseases, as it can inhibit the production of inflammatory mediators in activated BV-2 microglial cells.

Microglia have multiple functions in regulating homeostasis of the central nervous system. Microglia cells have been implicated as active contributors to neuron damage in neurodegenerative disorders. In this study, medicinal plant extracts (MPEs) were used to evaluate the cell-death induction effect in microglia BV-2 cells. Among 35 MPEs tested in this study, 4 MPEs showed less than a 30% cell survival after 24 hours of incubation. These were Foeniculi Fructus, Forsythiae Fructus, Zingiberis Rhizoma and Hedera Rhombea. The concentration showed that 50% cell death (IC50) occurred with 33, 83, 67 Ed highlight: Please confirm wording, and 81 μ /ml, respectively. For further study, we chose Zingiberis Rhizoma (ZR) which showed a reasonably low IC50 value and an induction of cell death in a relatively narrow range. Western blot analysis showed that ZR-treated cells showed activation of caspase-3 and cleavage of PARP Ed highlight: When an acronym is first presented it needs to be spelled out in both dose- and time-dependent manners. However, the level of Bcl-2 and Bax were not changed by ZR-treatment in BV-2 cells. These results suggest that ZR-induced apoptosis in BV-2 cells occured through caspase-3 activation. The results also suggested that ZR may be useful in developing treatments for neurodegenerative diseases.

[Background] Cordyceps militaris, a traditional medicinal mushroom, produces a component compound, cordycepin (3’-deoxyadenosine). Cordycepin has been known to have many pharmacological activities including immunological stimulating, anti-cancer, and anti-infection activities. However, the molecular mechanisms of inflammatory mediator’s activity by cordycepin remain poorly understood. In the present study, we investigat-ed the effects of cordycepin on the anti- inflammation cascades in lipopolysaccharide (LPS)-stimulated BV2 microglia cells. [Methods] Cordycepin were administered and their effects on LPS-induced pro-inflammatory mediators and MAP kinases were monitored by Western blotting and RT-PCR analysis. [Result] Cordycepin significantly inhibited the production of nitric oxide (NO), prostaglandin E2 (PGE2), and pro- inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in a concentration- dependent manner without causing cytotoxicity. Also, cordycepin suppressed inducible NO, synthase (iNOS) and cyclooxygenase-2 (COX-2) expression on the mRNA and protein level. In addition, cordycepin suppressed NF-κB translocation by blocking IkappaB- α (IκB-α) degradation and inhibited the phosphorylation of Akt, ERK-1/2, JNK, and p38 kinase. Our results indicate that the inhibitory effect of cordycepin on LPS -stimulated inflammatory mediator production in BV2 microglia is associated with the suppression of the NF-κB, Akt, and MAPK signaling pathways. Conclusion: Anti-inflammatory properties of cordycepin may be useful for treating the inflammatory and deleterious effects of microglial activation in response to LPS stimulation.