Abstract
The anti‐inflammatory effect of thalidomide has been well established. The mechanism of this anti‐inflammatory action is still not completely understood. Certain drugs exert their anti‐inflammatory action by stabilizing the membranes of polymorphonuclear neutrophils (PMN) thereby reducing the production of reactive oxygen intermediates. We evaluated the effect of thalidomide on cell membranes by using red blood cells (RBC), PMN and the monocyte‐like cell line THP‐1. Osmotic fragility of RBC showed that in vitro, thalidomide stabilized the membrane of RBC from plasma free blood; whereas, it did not affect RBCs from whole blood. Red blood cells taken from subjects before and after ingestion of thalidomide were not affected after exposure to different concentrations of hypotonic NaCl solution. Thalidomide did not affect the membrane stability of PMNs as well as THP‐1 in a significant manner. These data suggest that the anti‐inflammatory mechanism of thalidomide is not related to events associated with the oxidative burst of PMNs or monocytes.
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