Fraxin in Combination with Dexamethasone Attenuates LPS-Induced Liver and Heart Injury and Their Anticytokine Activity in Mice.

Background: Cytokine storm syndrome (CSS) is a major cause of morbidity and mortality in people suffering from hyperinflammatory status, which diverse etiological factors, including pathogens, therapeutic interventions, malignancies, and autoimmune disorders, can instigate. Since there is limited research on the antioxidant properties of fraxin and no studies have investigated its potential as an anticytokine storm agent, it is important to note that most studies have primarily focused on proinflammatory cytokines such as IL-1 Methods: Five groups of ten mice were randomly assigned: LPS only group (5 mg/kg, intraperitoneally i.p.), control (normal saline N.S. 1 ml/kg, i.p.), concentrations were selected based on previous literature, fraxin (120 mg/kg, i.p.), dexamethasone (5 mg/kg, i.p.), fraxin + dexamethasone (FD) (60 mg/kg + 2.5 mg/kg, i.p.), administered one hour before LPS injection (5 mg/kg,i.p.), animals were euthanized next day, and interleukin-8 (IL-8) was quantified in serum using an enzyme-linked immunosorbent assay. The liver and heart tissues underwent histopathological analysis to assess morphological changes. For data analysis using ANOVA and Tukey post hoc tests, the Kruskal-Wallis and Mann-Whitney Results: A significant decline in IL-8 levels was recorded in the treatment groups almost to the same degree ( Conclusions: All interventions used in this study significantly reduced interleukin-8 (IL-8) levels and reduced LPS-induced liver and cardiac damage. The combination (FD) did not result in an evident superiority of either agent. More research is required to identify the possible usefulness of these agents in treating hyperinflammatory diseases, such as cytokine storms, in future clinical practice.