Nicotine inhibits cardiac apoptosis induced by lipopolysaccharide in rats
Jun Suzuki, MD, PhD*,
Evelyn Bayna, PhD*,
Erminia Dalle Molle* and
Wilbur Y. W. Lew, MD, FACC*,*
* Cardiology Section, Department of Medicine, V.A. San Diego Healthcare System and University of California, San Diego, California, USA
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Figure 1 Terminal deoxy-nucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining in the left ventricle (mean ± SE, n = 5 to 7) of rats pretreated for 7 to 10 days with nicotine (6 mg/kg/day) versus saline (miniosmotic pump) and then injected with intravenous lipopolysaccharide (LPS) (1 mg/kg) versus vehicle. After 24 h, LPS increased TUNEL staining in saline pretreated rats (*p < 0.05, saline-LPS compared with other three groups).
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Figure 2 Terminal deoxy-nucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining (mean ± SE, n = 13) in cardiac myocytes isolated from rats pretreated for 7 to 10 days with nicotine (6 mg/kg/day) versus saline, and then exposed to lipopolysaccharide (LPS) (10 ng/ml) versus vehicle for 24 h. The LPS increased TUNEL staining in myocytes from saline pretreated rats (*p < 0.05, saline-LPS compared with other three groups).
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Figure 3 Toll-like receptor 4 (TLR4) messenger ribonucleic acid (mRNA) (normalized to 18 S ribosomal ribonucleic acid [rRNA]; mean ± SE, n = 4 to 6) in the heart after lipopolysaccharide (LPS) (1 mg/kg intravenously) injected into rats pretreated for 7 to 10 days with nicotine (6 mg/kg/day) versus saline. Toll-like receptor 4 mRNA increased at 8 to 16 h (*p < 0.05) with no difference between nicotine and saline pretreated rats. Open bar = saline; closed bar = nicotine.
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Figure 4 Angiotensinogen messenger ribonucleic acid (mRNA) (normalized to 18 S ribosomal ribonucleic acid [rRNA]; mean ± SE, n = 4 to 6) in the heart after lipopolysaccharide (LPS) (1 mg/kg intravenously) injected into rats pretreated for 7 to 10 days with nicotine (6 mg/kg/day) versus saline. Angiotensinogen mRNA increased at 8 h (*p < 0.05), with no difference between nicotine and saline pretreated rats. Open bar = saline; closed bar = nicotine.
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Figure 5 Terminal deoxy-nucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining (mean ± SE, n = 10 to 11) in cardiac myocytes isolated from rats pretreated for 7 to 10 days with nicotine (6 mg/kg/day) versus vehicle. In myocytes from saline-pretreated rats, TUNEL staining increased 24 h after lipopolysaccharide (LPS) (10 ng/ml) or angiotensin II (Ang II) (100 nM) compared with vehicle, but only Ang II had an effect in myocytes from nicotine-pretreated rats (*p < 0.05).
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Figure 6 Terminal deoxy-nucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining (mean ± SE, n = 10) in cardiac myocytes pretreated for 1 h with nicotine (15 ng/ml) versus saline. After 24 h, lipopolysaccharide (LPS) (10 ng/ml) increased TUNEL staining (*p < 0.05). This was attenuated, but not abolished by pretreatment of myocytes with nicotine for 1 h (+p < 0.05).
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