This paper introduce a way to prepare Guizhou palygorskite mineral nanoparticles by
dry-wet ball milling and modified its surface, with adding it in pre-polymer and dispersing with
supersonic disperser. Then it introduced preparing the tung oil phenolic-formaldehyde (TPF)/
nano-palygorskite composite resin by situ. The TENSOR27 IR and JEM-2000FX II test shown that
the nano-palygorskite particles embedded in the polymer and they were more evenly dispersed. By
NETZSCHSTA409 thermal analyzer for TG analysis, the elevated of compound PF has been
enhanced.
Aim: Indoleamine 2, 3-dioxygenase (IDO) is responsible for the progression of the kynurenine pathway, which has been implicated in the pathophysiology of inflammation-induced depression. It has been reported that asperosaponin Ⅵ (ASA Ⅵ) could play a neuroprotective role through anti-inflammatory and antioxidant. In this study, we examined the antidepressant effect of ASA Ⅵ in LPS-treated mice and further explored its molecular mechanism by insight into the microglial kynurenine pathway.
Methods: To produce the model, lipopolysaccharide (LPS) (0.83 mg/kg) was administered intraperitoneally to mice. The mice received ASA Ⅵ (10 mg/kg, 20mg/kg, 40mg/kg and 80mg/kg, i.p.) thirty minutes prior to LPS injection. Depressive-like behaviors were evaluated based on the duration of immobility in the forced swim test. Microglial activation and inflammatory cytokines were detected by immunohistochemistry, real-time PCR and ELISA. The TLR4/NF-ĸB signaling pathway and the expression of IDO, GluA2, and CamKIIβ were measured by western blotting. Results: ASA Ⅵ demonstrated significant antidepressant activity in the presence of LPS on immobility and latency times in the forced swim test. The LPS-induced activation of microglia and inflammatory response were inhabited by ASA Ⅵ in a dose-dependent manner. TLR4/NF-κB signaling pathway also was suppressed by ASA Ⅵ in the hippocampus and prefrontal cortex of LPS-treated mice. Furthermore, ASA Ⅵ inhibited the increase in IDO protein expression and normalized the aberrant glutamate transmission in the hippocampus and prefrontal cortex as a result of LPS administration. Conclusion: Our results propose a promising antidepressant effect for ASA Ⅵ possibly through the downregulation of IDO expression and normalization of the aberrant glutamate transmission. This remedying effect of ASA Ⅵ could be attributed to suppress microglia-mediated neuroinflammatory response via inhibiting the TLR4/NF-κB signaling pathway.
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