Effect of dimethyl sulfone on anti-inflammatory and immune function in mice

Objective:To investigate the effects of dimethyl sulfone on serum cytokines and the ability of carbon clearance in mice induced by lipopolysaccharide (LPS), and explore the anti-inflammatory effect of dimethyl sulfone and its effect on immune function.Methods:The mice were randomly divided into six groups including control group, model group, dexamethasone positive group and dimethylsulfone high, medium and low dose groups. After being continuously administrated for 7 d, the mice were injected with LPS intraperitoneally. The IL -17F, IL-22, IL-23 and TNF-α of serum were texted, and the spleen, thymus coefficient and the ability of carbon monocyte-macrophage carbon clearance in each group were calculate, respectively.Results: Compared with the model group, dimethyl sulfone group could significantly reduce the secretion of proinflammatory cytokines IL-17F and TNF-α, enhance the expression of anti-inflammatory factor IL-22 and significantly increase the phagocytosis rate of macrophages.Conclusion: Dimethyl sulfone has obvious anti-inflammatory effect on LPS-induced inflammatory mice and enhances immune function in mice, and it has no obvious inhibitory effect on immune system.

Preliminary study on the anti-inflammatory effect of magnolol on LPS-induced mice

Objective:Investigating the anti-inflammatory effects of magnolol on lipopolysaccharide (LPS)-induced inflammation model mouse and its effect on NF-κB pathway.Methods:Mice were randomly divided into 5 group: normal control group, inflammatory model group, dexamethasone positive drug group and, magnolol group. After administrating for 7 d, LPS was intraperitoneally injected to induce inflammatory on the 8th day, and blood was taken 3 h later and the thymus and spleen were weighed. The levels of serum TNF-α, IL-22 and IL-17 were detected by ELISA method. The expression levels of TNF-α, NF-κB p65 and IL-17 in thymus were detected by immunohistochemistry.Results: Magnolol could evidently reduce the levels of serum TNF-α, NF-κB p65 and IL-17 and IL-22. Immunohistochemistry result showed that magnolol could down-regulate the expression of IL-17, TNF-α and p65. Conclusion: Magnolol can prevent and treat LPS-induced inflammation. Its anti-inflammatory effect is connected with the down-regulation of TNF-α and NF-κB p65 protein levels by IL-17 inflammatory pathway. This experiment provides a theoretical basis for magnolol in anti-inflammatory.