A calpain inhibitor elevated expressions of NF-kappa B in atrial fibrillation canine atria

This aim of this study is to observe the alterations of calpain proteolytic system and effect of a calpain I inhibitor on NF-kappa B expressions in rapid pacing canine atrial fibrillation (AF) models. Twenty-one dogs were divided equally into three groups: a sham operation group, a control AF group and a calpain inhibitor group. Rapid right atrium pacing at 600 beats per min was applied in the control AF group and the calpain inhibitor group. N-Acetyl-Leu-Leu-Met (1.0 mg/kg/day) was administered in the calpain inhibitor group for three weeks. The protein expressions of NF-kappa B, calpain I, calpain II and calpastatin were assessed by immunohistochemistry and gene amplification of NF-kappa B and calpain I were detected by quantitative real time polymerase chain reaction. The highest density of calpain I was shown in the control AF group (p < 0.01, vs. calpain inhibitor group and sham operation group). Protein expression of calpain II and calpastatin had no significant difference among the three groups. Gene amplification results of calpain I unveiled the most active transcription was in the calpain inhibitor group (p < 0.01, vs. control AF group and sham operation group). The mRNA expression of NF-kappa B were elevated in the calpain inhibitor group, the cycle of threshold means were (20.1 +/- 5.1), while were (33.4 +/- 6.1) and (30.4 +/- 5.8) in the sham operation group and control AF group, respectively. NF-kappa B protein expressions in calpain inhibitor group were positive, while were negative in the other two groups. In canine heart muscle cells, atrial fibrillation elevated calpain I gene transcription, promoted protein expression and enhanced protease activity. The calpain I inhibitor N-Acetyl-Leu-Leu-Met promoted NF-kappa B gene transcription and protein expressions in AF canine models.