Figure 7.

Pharmacologic inhibition of calpain and genetic deletion of Capn1 mitigate diabetes-induced iNOS, ICAM-1 up-regulation, and pIκBα. A, D, and G: Calpain inhibitor was administered daily to diabetic mice (i.p. daily 10 mg/kg). B and E: Whole-body deletion of Capn1. Duration of diabetes was 2 months at the time of this assay, and administration of the inhibitor began promptly after the initiation of diabetes (n = 4 to 7 per group). C, F, and H: Representative immunoblots for iNOS, ICAM-1, β-actin, pIκBα, and IκBα. A, B, D, E, and G: Summary graph of data for iNOS, ICAM-1, and pIκBα expression determined by image analysis. Data are expressed relative to the expression of β-actin, a housekeeping protein, and IκBα in the. same lanes, for iNOS and ICAM, and for pIκBα, respectively. Data are expressed as a percentage of the value of nondiabetic controls. ∗P ≤ 0.05; ∗∗P ≤ 0.01; and ∗∗∗P ≤ 0.001. D, diabetic; ICAM-1, intercellular adhesion molecule 1; iNOS, inducible nitric oxide synthase; N, nondiabetic.