Modulation Of Catalpol On Inflammatory Reaction Induced By Lipopolysacchride

Bacterial lipopolysaccharide (LPS), an inducer of immunological inflammation, was used to establish the inflammatory model in vivo, and the protective effect of catalpol was evaluated in lipopolysaccharide-induced inflammatory mice via behavioral immunological function and mitochondrial function.Mice were injected intraperitoneally (i.p.) with LPS 100μg/mouse to establish acute inflammatory model. Effects of catalpol on the cognition ability of LPS-induced inflammatory mice were evaluated by Morris water maze. The results showed that injection of LPS caused the degression of cognitive ability. Catalpol pretreatment for ten days was capable of reversing the LPS-induced behavioral impairment. In order to make clear the neuroprotective mechanism of catalpol on inflammatory model induced by LPS, HE staining showed that pyramidalneurons either presented a densely stained shrunken appearance with minimal cytoplasm or had disappeared in the brain of LPS-induced inflammatory mice. In contrast, majority of the neurons were rescued in mice pretreated with catalpol. Using biochemistry method found that expression of NFκB, the production of related inflammatory factors including ROS, iNOS, and the degree of MPTP opening were increased, and the activity ofΔΨwas decreased in LPS-induced inflammatory mice. In contrast, the neurons were rescued in mice pretreatment with catalpol. Moreover, catalpol pretreatment decreased the expression of NFκB, the production of related inflammatory factors including ROS, iNOS, and the degree of MPTP opening, and increased the activity ofΔΨ, and eventually ameliorated cognition deficits of LPS-induced inflammatory mice. Furthermore, the weight and spleen indices were assayed. The data indicated that catalpol significantly elevated the weight and spleen indices, suggesting that catalpol could protect mice from LPS induced damage by modulating immunological function.In summary, the results suggested that catalpol protected LPS-induced inflammatory mice from damage and might exert its protection by decreasing the production of inflammatory factors and modulating mitochondrial function.