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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2014 Mar 6;34(5):966–975. doi: 10.1161/ATVBAHA.113.302484

Figure 2. SR-BI controls inducible GC generation in response to septic stress, but supplementation of GC only partly restored GC-induced thymocyte apoptosis in SR-BI−/− mice.

Figure 2

A) Lack of inducible GC production in SR-BI−/− mice in sepsis. SR-BI+/+ and SR-BI−/− mice were subjected to CLP (22G needle, full ligation) for 2 h and the serum corticosterone levels were quantified. n = 6 per group; B and C) Supplementation of dexamethasone only partly restored GC-induced thymocyte apoptosis in SR-BI−/− mice. SR-BI+/+ and SR-BI−/− mice were administered Dex (8mg/kg body weight, i.p.) for18 h. Thymocyte apoptosis was analyzed by DNA ladder assay (B) and by TUNEL assay (C). n = 8–10 per group.