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. 2013 May 17;62(6):2078–2087. doi: 10.2337/db12-1374

FIG. 3.

FIG. 3.

Effect of the NF-kB inhibition on EDR in MRAs. Key representative traces showing EDR curves to ACh from control and type 2 diabetic mice (db/db) treated with or without DHMEQ or IKK-NBD peptide, db/db−p50NF-kB−/− mice, and db/db−PARP-1−/−) mice (A). EDR in response to cumulative doses of ACh (10−8 to 10−5 mol/L) in MRAs precontracted with PE (10−5 mol/L) from control and db/db treated with or without DHMEQ or IKK-NBD peptide (B) and incubated with or without apocynin (Apo) (NADPH oxidase inhibitor) (C) or NS 398 (COX-2 inhibitor) (D). *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. EDR in MRA from control, db/db, db/db−p50NF-kB−/−, and db-/db-PARP-1−/− (E) and incubated with COX-2 inhibitor, NS 398 (F), and db/db incubated with either AG1478 (EGFRtk inhibitor) (G) or P65NF-kB shRNA lentiviral particles (H). *P < 0.05 for db/db vs. control, db/db−p50NF-kB−/−, or db/db−PARP-1−/−. #P < 0.05 for db/db−PARP-1−/− vs. control, db/db−p50NF-kB−/−. $P < 0.05 for db/db vs. db/db plus AG1478. @P < 0.05 for db/db, db/db plus scrambled vs. db/db plus p65 shRNA.