Figure 14.

NF‐κB inhibition attenuates cardiomyocyte hypertrophy and interstitial fibrosis at 2 weeks after TAC. A through D, Mice were analyzed at 2 weeks after TAC or sham operation under treatment of an NF‐κB inhibitor (NF‐κBI) or vehicle. A, Hematoxylin and eosin–stained heart sections. Cardiomyocyte cross‐sectional area was measured in 20 cardiomyocytes (n=3). Scale bars=20 μm. B, Sirius Red–stained heart sections. Collagen volume fraction was calculated in 5 random fields (n=3). Scale bars=50 μm. C, Expression of hypertrophic marker genes. Expression levels of atrial natriuretic factor (Anf) and β‐myosin heavy chain (β‐Mhc) mRNAs were measured (n=3). D, Expression of fibrosis‐related genes. Expression levels of collagen type 1 α1 (Col1a1), collagen type 3 α1 (Col3a1), and transforming growth factor‐β1 (Tgfβ1) mRNAs were measured (n=3). Expression levels of each gene were normalized to those of GAPDH (Gapdh). *P<0.05 vs sham; ^†P<0.05 vs vehicle. NF indicates nuclear factor; GAPDH, glyceraldehyde‐3‐phosphate dehydrogenase; TAC, transverse aortic constriction.