Abstract

Objective: This study examined whether cytokine response accompanied by sublethal hemorrhage (SLH) might be modified by treatment with magnolol. Methods: Rats were randomly segregated into three experimental groups. The control group rats received sham-operations and vehicle treatment. The untreated group rats received SLH and vehicle treatment. The treated group rats received SLH and magnolol treatment. All animals were subjected to subsequent lethal endotoxin challenge 24 hours later. Plasma TNF-alpha and IL-l0 levels, lipid peroxidation, and superoxide dismutase (SOD) activity in the lung were measured following SLU or endotoxin challenge. Results: Plasma TNF-alpha increased after SLH in both the treated and untreated groups, whereas a significant lower level was noted in the treated group compared with the untreated group. After endotoxin sepsis, blunting of the TNF-alpha levels were found in both the treated and untreated groups. The plasma IL-l0 level increased significantly in the treated group compared with that in the untreated and control groups. Lipid peroxidation and SOD activity increased after SLH in the untreated group. Magnolol suppressed the lipid peroxidation but not the SOD activity. After endotoxin, lipid peroxidation was higher in the control group compared with that in the treated and untreated groups. Survival analysis showed that outcome was not different between the treated and untreated groups. Conclusion: Magnolol modifies the response of cytokines and decreases their oxidative activity after SLH. Magnolol increases IL-l0 response and preserves SOD activity after SLH, although the final outcome after subsequent endotoxin challenge is not altered significantly.

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