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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

Anti-inflammatory effects of individual HIPER components. HCAECs were treated with HIPER or pine bark extract (PBE), papain (Pap), honey (Hon), or aloe vera (AV) for 3 h and then activated with 1 ng/mL TNF-α for 1 h. Total RNA was extracted and VCAM-1 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, and ∗∗P < 0.05 HIPER versus PBE.
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fig6: Anti-inflammatory effects of individual HIPER components. HCAECs were treated with HIPER or pine bark extract (PBE), papain (Pap), honey (Hon), or aloe vera (AV) for 3 h and then activated with 1 ng/mL TNF-α for 1 h. Total RNA was extracted and VCAM-1 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, and ∗∗P < 0.05 HIPER versus PBE.

Mentions: To test each HIPER ingredient for an individual anti-inflammatory effect, HCAECs were exposed to either PBE (130 μg/mL or 260 μg/mL), aloe vera (1.75 mg/mL), honey (0.1%), or papain (2.4 mg/mL) for 3 h before being activated with TNF-α (1 ng/mL) for a further 3 h. The anti-inflammatory effect of each individual component was compared to each other and to the parent compound, HIPER (25 μL/mL). Figure 6 shows that HIPER (25 μL/mL) and PBE (at both concentrations) decreased TNF-α-induced VCAM-1 mRNA levels. PBE was twice as effective as HIPER in decreasing TNF-α-induced VCAM-1 expression (1.5-fold versus 3-fold, resp., P < 0.05). Honey and aloe vera showed a nonsignificant trend towards decreased VCAM-1 mRNA levels. By contrast, papain increased VCAM-1 mRNA levels (1.5-fold, P < 0.05) over and above expression levels induced by TNF-α.


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)

Anti-inflammatory effects of individual HIPER components. HCAECs were treated with HIPER or pine bark extract (PBE), papain (Pap), honey (Hon), or aloe vera (AV) for 3 h and then activated with 1 ng/mL TNF-α for 1 h. Total RNA was extracted and VCAM-1 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, and ∗∗P < 0.05 HIPER versus PBE.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4664804&req=5

fig6: Anti-inflammatory effects of individual HIPER components. HCAECs were treated with HIPER or pine bark extract (PBE), papain (Pap), honey (Hon), or aloe vera (AV) for 3 h and then activated with 1 ng/mL TNF-α for 1 h. Total RNA was extracted and VCAM-1 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, and ∗∗P < 0.05 HIPER versus PBE.
Mentions: To test each HIPER ingredient for an individual anti-inflammatory effect, HCAECs were exposed to either PBE (130 μg/mL or 260 μg/mL), aloe vera (1.75 mg/mL), honey (0.1%), or papain (2.4 mg/mL) for 3 h before being activated with TNF-α (1 ng/mL) for a further 3 h. The anti-inflammatory effect of each individual component was compared to each other and to the parent compound, HIPER (25 μL/mL). Figure 6 shows that HIPER (25 μL/mL) and PBE (at both concentrations) decreased TNF-α-induced VCAM-1 mRNA levels. PBE was twice as effective as HIPER in decreasing TNF-α-induced VCAM-1 expression (1.5-fold versus 3-fold, resp., P < 0.05). Honey and aloe vera showed a nonsignificant trend towards decreased VCAM-1 mRNA levels. By contrast, papain increased VCAM-1 mRNA levels (1.5-fold, P < 0.05) over and above expression levels induced by TNF-α.

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