<abstract xmlns="http://www.w3.org/1999/xhtml"> 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 &lt;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&lt;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 &lt;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. </abstract>

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.

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

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060,

Department of Geriatrics, Renmin Hospital of Wuhan University, Wuhan 430060,

Asian Biomedicine

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

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, 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.

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

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

Article Category: Original article

Online veröffentlicht: 04. Feb. 2017

Seitenbereich: 343 - 350

DOI: https://doi.org/10.5372/1905-7415.0603.065

Schlüsselwörter
Lactate dehydrogenase, macrophage, nicotine, tumor necrosis factor-α

© 2017

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

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

Article Category: Original article

Online veröffentlicht: 04. Feb. 2017

Seitenbereich: 343 - 350

DOI: https://doi.org/10.5372/1905-7415.0603.065

SchlüsselwörterLactate dehydrogenase, macrophage, nicotine, tumor necrosis factor-α

© 2017

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

Schlüsselwörter
Lactate dehydrogenase, macrophage, nicotine, tumor necrosis factor-α