Effect of nicotine on the release of lactate dehydrogenase and the production of tumor necrosis factor-α of cultured macrophage

Background: Nicotine can affect the development of Atherosclerosis (AS). Monocytes/macrophages are the important cells hi the AS lesions.

Objective: We studied the mechanisms of smoking on AS. The effects of nicotine on macrophage were investigated hi this study.

Methods: Different concentration of nicotine (6 × 10^-9~-5 mol/L), different incubation time (3, 6, 9, 12, 18, and 24 horn s) and 7 β-hydroxycholesterol (50 μg ml) were schemed in this study. After exposure of macrophage to those different conditions, lactate dehydrogenase (LDH) activity and tumor necrosis factor-⃞ (TNF-α) content in the supernatant were assayed.

Results: Nicotine (6 × 10^-9mol/L~-6×10^-5mol/L) treatment resulted in a marked reduction of LDH in the supernatant (131,0±9.6 U/L. 129.7±6.2 U/L, 129.4±5.3 U/L, 134.2±8.4 U/L, and 138.3+9.7 U/L vs. 151.3+8.1 U/L, p <0.05 respectively, q-test). The same change trend was seen when co-treated with 7β-hydroxycholestrol and nicotine (135.7±7.6U/L, 135.6±6.6U/L, 136.1±6.7 U/L, 142.9±4.5 U/L, and 146.4±4.4 U/L vs. 152.4⃞6.2U/L, P<0.05 respectively, q-test). The peak effects occurred at the nicotine concentration of 6 × 10^-7mol/L and the first 18-hours incubation. Nicotine (6 ×10^-9mol/L~6 × 10^-6mol L) treatment result in the increase of TNF-α in the supernatant (0.28±0.06 ng/mL, 0.32±0.05 ng/mL, 0.40±0.07 ng/mL. and 0.30±0.08 ng/mL vs. 0.17±0.05 ng/mL, p <0.05 respectively, q-test). Nicotine (6 × 10^-5mol/L) treatment have no significant hicrease compared to the control group (0.21±0.08 ng/mL vs. 0.17+0.05 ng/mL, p >0.05, q-test). The peak effects occurred at the nicothie concentration of 6 × 10^-7mol/L.

Conclusions: Nicotine can produce the beneficial effect on macrophage. Nicotine treatment can activate macrophage to produce TNF-α. Thus, nicotine can be a mechanism on the development of atherosclerosis.