Steroids inhibit activation of the alternative-amplification pathway of complement.
Previous studies have demonstrated the ability of methylprednisolone sodium succinate to inhibit complement activation. Two other glucocorticosteroids and three different soluble steroids which lacked glucocorticoid activity were found in the present study to have the capacity to inhibit lysis of sheep erythrocytes by the alternative-amplification pathway. These compounds also inhibited fluid-phase consumption of B in a reaction mixture that contained purified C3b, B, and D, indicating that they exert a direct effect on the generation of alternative amplification pathway convertase. These findings suggest that the capacity to inhibit convertase generation by glucocorticosteroids in high concentration is independent of glucocorticoid activity.
D003167:Complement Activation / Q000187:drug effects*; D050577:Complement C3-C5 Convertases / Q000378:metabolism; D003170:Complement Pathway, Alternative / Q000187:drug effects*; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D005999:Glycochenodeoxycholic Acid / Q000494:pharmacology; D006854:Hydrocortisone / Q000494:pharmacology; D008776:Methylprednisolone Hemisuccinate / Q000494:pharmacology; D011239:Prednisolone / Q000031:analogs & derivatives / Q000494:pharmacology; D013256:Steroids / Q000494:pharmacology*; D013329:Structure-Activity Relationship; D013739:Testosterone / Q000031:analogs & derivatives / Q000494:pharmacology
D013256:Steroids; C031555:estradiol sulfate; D013739:Testosterone; D004958:Estradiol; D008776:Methylprednisolone Hemisuccinate; D005999:Glycochenodeoxycholic Acid; C028627:testosterone-17-sulfate; C009022:prednisolone phosphate; D011239:Prednisolone; D050577:Complement C3-C5 Convertases; D006854:Hydrocortisone