Functional benefits of corticosteroid and IVIG combination therapy in a coronary artery endothelial cell model of Kawasaki disease

摘要

DEX, but not high-dose IgG, inhibits cellular damage to, and HMGB1 protein release by, HCAECs in response to inflammatory stimuli. HCAECs were stimulated with 100 ng/ml of TNF-α, or 10 ng/ml of IL-1α or IL-1β, for 24 h in the presence and absence of 10 mg/ml IgG and 1000 nM DEX, alone or in combination. Protein concentrations of HMGB1 in the culture supernatants (a), and HMGB1 mRNA levels (b) and caspase 3/7 activities in HCAECs (c) were measured by ELISA, qPCR and the Caspase-Glo 3/7 Assay System, respectively. Data are shown as the mean ± SD of triplicate samples and are representative of two individual experiments using HCAEC lots from different donors. **P < 0.01 compared with 100 ng/ml TNF-α; ††P < 0.01 compared with 10 ng/ml IL-1α; and ‡‡P < 0.01 compared with 10 ng/ml IL-1β