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Inhibitory Effect of a French Maritime Pine Bark Extract-Based Nutritional Supplement on TNF-α-Induced Inflammation and Oxidative Stress in Human Coronary Artery Endothelial Cells.

McGrath KC, Li XH, McRobb LS, Heather AK - Evid Based Complement Alternat Med (2015)

Bottom Line: Treatment for 24 hours with HIPER reduced TNF-α-induced reactive oxygen species (ROS) generation that was associated with decreased NADPH oxidase 4 and increased superoxide dismutase-1 expression.HIPER inhibited TNF-α induced monocyte adhesion to HCAECs that was in keeping with decreased expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 and decreased nuclear factor-kappa B (NF-κB) activation.Further investigation of mechanism showed HIPER reduced TNF-α induced IκBα and p38 and MEK1/2 MAP kinases phosphorylation.

View Article: PubMed Central - PubMed

Affiliation: Molecular Biosciences Team, School of Life Sciences, University of Technology Sydney, Broadway, NSW, Australia.

ABSTRACT
Oxidative stress and inflammation, leading to endothelial dysfunction, contribute to the pathogenesis of atherosclerosis. The popularity of natural product supplements has increased in recent years, especially those with purported anti-inflammatory and/or antioxidant effects. The efficacy and mechanism of many of these products are not yet well understood. In this study, we tested the antioxidant and anti-inflammatory effects of a supplement, HIPER Health Supplement (HIPER), on cytokine-induced inflammation and oxidative stress in human coronary artery endothelial cells (HCAECs). HIPER is a mixture of French maritime pine bark extract (PBE), honey, aloe vera, and papaya extract. Treatment for 24 hours with HIPER reduced TNF-α-induced reactive oxygen species (ROS) generation that was associated with decreased NADPH oxidase 4 and increased superoxide dismutase-1 expression. HIPER inhibited TNF-α induced monocyte adhesion to HCAECs that was in keeping with decreased expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 and decreased nuclear factor-kappa B (NF-κB) activation. Further investigation of mechanism showed HIPER reduced TNF-α induced IκBα and p38 and MEK1/2 MAP kinases phosphorylation. Our findings show that HIPER has potent inhibitory effects on HCAECs inflammatory and oxidative stress responses that may protect against endothelial dysfunction that underlies early atherosclerotic lesion formation.

No MeSH data available.


Related in: MedlinePlus

HIPER modulated NOX4 and SOD1 mRNA levels in TNF-α-activated HCAECs. HCAECs were treated with HIPER at concentrations of 6.25, 12.5, 25, and 50 μL/mL for 3 h, before activation with 1 ng/mL TNF-α for 1 h. Total RNA was extracted and NOX4 (a) and SOD-1 (b) mRNA levels were measured by RT-qPCR. Data are shown as mean ± SEM (n = 3). #P < 0.05 versus control, ∗P < 0.05 versus TNF-α.
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fig2: HIPER modulated NOX4 and SOD1 mRNA levels in TNF-α-activated HCAECs. HCAECs were treated with HIPER at concentrations of 6.25, 12.5, 25, and 50 μL/mL for 3 h, before activation with 1 ng/mL TNF-α for 1 h. Total RNA was extracted and NOX4 (a) and SOD-1 (b) mRNA levels were measured by RT-qPCR. Data are shown as mean ± SEM (n = 3). #P < 0.05 versus control, ∗P < 0.05 versus TNF-α.

Mentions: TNF-α treatment increased NADPH oxidase 4 (NOX4) expression by 15%, a result that was abrogated in HCAECs pretreated with 25 or 50 μL/mL HIPER for 3 h (Figure 2(a); P < 0.05). In contrast, TNF-α decreased superoxide dismutase-1 (SOD-1) expression by 24% (Figure 2(b); P < 0.05), which was also abrogated by HIPER pretreatment at both the 25 and 50 μL/mL concentrations (P < 0.05).


Inhibitory Effect of a French Maritime Pine Bark Extract-Based Nutritional Supplement on TNF-α-Induced Inflammation and Oxidative Stress in Human Coronary Artery Endothelial Cells.

McGrath KC, Li XH, McRobb LS, Heather AK - Evid Based Complement Alternat Med (2015)

HIPER modulated NOX4 and SOD1 mRNA levels in TNF-α-activated HCAECs. HCAECs were treated with HIPER at concentrations of 6.25, 12.5, 25, and 50 μL/mL for 3 h, before activation with 1 ng/mL TNF-α for 1 h. Total RNA was extracted and NOX4 (a) and SOD-1 (b) mRNA levels were measured by RT-qPCR. Data are shown as mean ± SEM (n = 3). #P < 0.05 versus control, ∗P < 0.05 versus TNF-α.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4664804&req=5

fig2: HIPER modulated NOX4 and SOD1 mRNA levels in TNF-α-activated HCAECs. HCAECs were treated with HIPER at concentrations of 6.25, 12.5, 25, and 50 μL/mL for 3 h, before activation with 1 ng/mL TNF-α for 1 h. Total RNA was extracted and NOX4 (a) and SOD-1 (b) mRNA levels were measured by RT-qPCR. Data are shown as mean ± SEM (n = 3). #P < 0.05 versus control, ∗P < 0.05 versus TNF-α.
Mentions: TNF-α treatment increased NADPH oxidase 4 (NOX4) expression by 15%, a result that was abrogated in HCAECs pretreated with 25 or 50 μL/mL HIPER for 3 h (Figure 2(a); P < 0.05). In contrast, TNF-α decreased superoxide dismutase-1 (SOD-1) expression by 24% (Figure 2(b); P < 0.05), which was also abrogated by HIPER pretreatment at both the 25 and 50 μL/mL concentrations (P < 0.05).

Bottom Line: Treatment for 24 hours with HIPER reduced TNF-α-induced reactive oxygen species (ROS) generation that was associated with decreased NADPH oxidase 4 and increased superoxide dismutase-1 expression.HIPER inhibited TNF-α induced monocyte adhesion to HCAECs that was in keeping with decreased expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 and decreased nuclear factor-kappa B (NF-κB) activation.Further investigation of mechanism showed HIPER reduced TNF-α induced IκBα and p38 and MEK1/2 MAP kinases phosphorylation.

View Article: PubMed Central - PubMed

Affiliation: Molecular Biosciences Team, School of Life Sciences, University of Technology Sydney, Broadway, NSW, Australia.

ABSTRACT
Oxidative stress and inflammation, leading to endothelial dysfunction, contribute to the pathogenesis of atherosclerosis. The popularity of natural product supplements has increased in recent years, especially those with purported anti-inflammatory and/or antioxidant effects. The efficacy and mechanism of many of these products are not yet well understood. In this study, we tested the antioxidant and anti-inflammatory effects of a supplement, HIPER Health Supplement (HIPER), on cytokine-induced inflammation and oxidative stress in human coronary artery endothelial cells (HCAECs). HIPER is a mixture of French maritime pine bark extract (PBE), honey, aloe vera, and papaya extract. Treatment for 24 hours with HIPER reduced TNF-α-induced reactive oxygen species (ROS) generation that was associated with decreased NADPH oxidase 4 and increased superoxide dismutase-1 expression. HIPER inhibited TNF-α induced monocyte adhesion to HCAECs that was in keeping with decreased expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 and decreased nuclear factor-kappa B (NF-κB) activation. Further investigation of mechanism showed HIPER reduced TNF-α induced IκBα and p38 and MEK1/2 MAP kinases phosphorylation. Our findings show that HIPER has potent inhibitory effects on HCAECs inflammatory and oxidative stress responses that may protect against endothelial dysfunction that underlies early atherosclerotic lesion formation.

No MeSH data available.


Related in: MedlinePlus