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. Author manuscript; available in PMC: 2016 Apr 12.
Published in final edited form as: Diabetes Metab Res Rev. 2015 Jan;31(1):39–49. doi: 10.1002/dmrr.2542

Figure 1. Effect of the NFκB inhibition on endothelium-dependent relaxation in thoracic aorta (n=10).

Figure 1

Key representative traces showing endothelium-dependent relaxation curves to ACh from control, and type 2 diabetic mice (db−/db−) treated with or without DHMEQ or IKK-NBD peptide and double knockout mice between db−/db− and p-50NFκB (db−/db-p-50NFκB−/−) and double knockout mice between db−/db− and PARP-1 male mice (db−/db-PARP-1−/−) (A). Endothelium-dependent relaxation in response to cumulative doses of ACh (10−8−3.10−5 M) in rings from aorta, pre-contracted with phenylephrine (PE, 10−5 M), from control, db−/db− treated with or without DHMEQ or IKK-NBD peptide (B) and incubated with apocynin (APO, NADPH oxidase inhibitor) (C) or NS 398 (COX-2 inhibitor) (D) or L-NAME (eNOS inhibitor) (E). Control, control treated with or without DHMEQ or IKK-NBD peptide (F). *P < 0.05 for db−/db− vs. control, db−/db− treated with DHMEQ or IKK-NBD. &P < 0.05 for db−/db− treated with DHMEQ or IKK-NBD vs. control.