The non-provitamin A carotenoid, lutein, inhibits NF-κB-dependent gene expression through redox-based regulation of the phosphatidylinositol 3-kinase/PTEN/Akt and NF-κB-inducing kinase pathways: Role of H2O2 in NF-κB activation

Kim, Jihee; Na, Hee Jun; Kim, Chun Ki; Kim, Ji Yoon; Ha, Kwon Soo; Lee, Hansoo; Chung, Hun Taeg; Kwon, Ho Jeong; Kwon, Young Guen; Kim, Young Myeong

doi:10.1016/j.freeradbiomed.2008.06.019

Cited by 232 publications

(183 citation statements)

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“…According to an earlier report, AKT serinethreonine kinase is involved in the activation of NF-kB (43). A recent study showed that lutein, an antioxidant, significantly attenuated LPS-evoked NF-kB activation and inflammatory gene expression through suppressing the PI3K/AKT signaling pathway (44). Indeed, the current study showed for the first time, to our knowledge, that maternal LPS exposure resulted in placental AKT phosphorylation.…”

Section: Discussionsupporting

confidence: 55%

Zinc Supplementation during Pregnancy Protects against Lipopolysaccharide-Induced Fetal Growth Restriction and Demise through Its Anti-inflammatory Effect

Chen

Zhao

Xue

et al. 2012

The Journal of Immunology

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LPS is associated with adverse developmental outcomes, including preterm delivery, fetal death, teratogenicity, and intrauterine growth restriction (IUGR). Previous reports showed that zinc protected against LPS-induced teratogenicity. In the current study, we investigated the effects of zinc supplementation during pregnancy on LPS-induced preterm delivery, fetal death and IUGR. All pregnant mice except controls were i.p. injected with LPS (75 μg/kg) daily from gestational day (GD) 15 to GD17. Some pregnant mice were administered zinc sulfate through drinking water (75 mg elemental Zn per liter) throughout the pregnancy. As expected, an i.p. injection with LPS daily from GD15 to GD17 resulted in 36.4% (4/11) of dams delivered before GD18. In dams that completed the pregnancy, 63.2% of fetuses were dead. Moreover, LPS significantly reduced fetal weight and crown–rump length. Of interest, zinc supplementation during pregnancy protected mice from LPS-induced preterm delivery and fetal death. In addition, zinc supplementation significantly alleviated LPS-induced IUGR and skeletal development retardation. Further experiments showed that zinc supplementation significantly attenuated LPS-induced expression of placental inflammatory cytokines and cyclooxygenase-2. Zinc supplementation also significantly attenuated LPS-induced activation of NF-κB and MAPK signaling in mononuclear sinusoidal trophoblast giant cells of the labyrinth zone. It inhibited LPS-induced placental AKT phosphorylation as well. In conclusion, zinc supplementation during pregnancy protects against LPS-induced fetal growth restriction and demise through its anti-inflammatory effect.

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Section: Discussionsupporting

confidence: 55%

Zinc Supplementation during Pregnancy Protects against Lipopolysaccharide-Induced Fetal Growth Restriction and Demise through Its Anti-inflammatory Effect

Chen

Zhao

Xue

et al. 2012

The Journal of Immunology

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“…NF-κB exists in the cytosol in an inactive form bound to an inhibitor IκB, and following inflammatory stimuli, intracellular signals activate the IκB kinase complex, in turn inducing phosphorylation and degradation of IκB from NF-κB. Activation of the NF-κB pathway results in the nuclear appearance of p50 and p65, and the subsequent transcriptional induction of genes associated with the production of inflammatory mediators and cytokines (Kim et al, 2008). While several ROS play a role in the activation of NF-κB, H2O2 specifically modulates NF-κB by promoting the activation of the NIK/IKK pathway (Kim et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Activation of the NF-κB pathway results in the nuclear appearance of p50 and p65, and the subsequent transcriptional induction of genes associated with the production of inflammatory mediators and cytokines (Kim et al, 2008). While several ROS play a role in the activation of NF-κB, H2O2 specifically modulates NF-κB by promoting the activation of the NIK/IKK pathway (Kim et al, 2008). HUVEC incubated in the presence of H2O2 showed an increase in nuclear p50 activity, indicating the upregulation of the NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin Decreases Inflammatory Biomarkers Associated with Cardiovascular Disease in Human Umbilical Vein Endothelial Cells

Chew¹,

Mathison²,

Kimble³

et al. 2013

AJAFST

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Oxidative stress and inflammation are strongly linked to the development of cardiovascular disease (CVD). As a potent antioxidant, astaxanthin may downregulate inflammation-associated factors involved in endothelial dysfunction and CVD progression. We studied the possible protective effects of astaxanthin against endothelial dysfunction in human umbilical vein endothelial cells (HUVEC) induced with hydrogen peroxide (H2O2). Cells were pre-incubated with 0, 0.01, 0.1, or 1.0 μmol/L astaxanthin for 48 h, then oxidative stress induced with 100 μmol/L H2O2 overnight. Uptake kinetics of astaxanthin showed a time-dependent uptake of astaxanthin (1.0 μmol/L) by HUVEC over the 48 h incubation period. Oxidative stress induction with H2O2 in HUVEC decreased intracellular antioxidant activity and increased the production of inflammatory biomarkers and reactive oxygen species (ROS). In contrast, pre-incubation of HUVEC with astaxanthin prior to H2O2 stress increased (P < 0.05) superoxide dismutase activity and decreased ROS, prostaglandin E2, leukotriene B4, NO, IL-8, and IFN- production. Pre-treatment with astaxanthin also downregulated the transcriptional activation of NF-κB and activator protein-1, thereby inhibiting downstream production of inflammatory mediators and cytokines. Therefore, astaxanthin protects against factors initiated by H2O2 addition, likely by scavenging ROS required for transcriptional activation and inhibiting the production of inflammatory biomarkers involved in endothelial dysfunction and CVD.Abbreviations: AP-1: activator protein-1; CVD: cardiovascular disease; CS: culture supernatant; EGM-2: endothelial growth medium-2; GPx: glutathione peroxidase; H2O2: hydrogen peroxide; HUVEC: human umbilical vein endothelial cell; LTB4: leukotriene B4; PGE2: prostaglandin E2; ROS: reactive oxygen species; SOD: superoxide dismutase; THF: tetrahydrofuran.

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“…These two hypotheses linking variation in plasma carotenoids and the immune response in a direct and indirect way are not mutually exclusive. Carotenoids exert important immunomodulatory functions that might be especially important in a PHA response, such as stimulating the production of cytokines and the activity of immune cells (reviewed by Chew, 1993;Møller et al, 2000), as well as regulating inflammation (Rafi and Shafaie, 2007;Kim et al, 2008). Changes in plasma carotenoid levels might therefore directly reflect their rapid re-allocation to immune tissues or cells (Koutsos et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Dynamics of PHA-induced immune response and plasma carotenoids in birds:should we have a closer look?

Biard

Hardy

Motreuil

et al. 2009

Journal of Experimental Biology

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SUMMARYAllocation trade-offs of limited resources are thought to ensure the honesty of sexual signals and are often studied using controlled immune challenges. One such trade-off between immunity and ornaments is that involving carotenoids. Phytohemagglutinin (PHA)-induced immune response is a widely used immune challenge, yet more details on the underlying physiological mechanisms and potential costs are needed. We investigated the temporal dynamics of PHA-induced immune response and associated changes in blood carotenoids, body mass and a carotenoid-based coloured signal. We found variation in individual response patterns to PHA after peak swelling was reached, with birds showing either a rapid or a slow subsequent decrease in swelling, suggesting variation in the duration of the immune response and/or inflammation. Body mass did not affect immune response. Plasma carotenoids followed a transient decrease closely matching the dynamics of the swelling. The peak of the immune response was negatively related to initial plasma carotenoid levels and positively correlated to the relative decrease in plasma carotenoids. Individual variation in duration of the swelling could be partly explained by plasma carotenoids; high initial carotenoid levels were associated with a slower decrease of the swelling. These contradictory effects of carotenoids suggest a complex role in the immune response. Bill colour was positively correlated to initial plasma carotenoid concentration but it did not predict or change as a consequence of immune response to PHA. Bill colour thus reflects medium-or long-term quality rather than immediate quality. Taking into account the dynamics of the immune response and that of associated physiological parameters would thus yield new insights into our interpretation of variation in PHA response.

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The non-provitamin A carotenoid, lutein, inhibits NF-κB-dependent gene expression through redox-based regulation of the phosphatidylinositol 3-kinase/PTEN/Akt and NF-κB-inducing kinase pathways: Role of H2O2 in NF-κB activation

Cited by 232 publications

References 47 publications

Zinc Supplementation during Pregnancy Protects against Lipopolysaccharide-Induced Fetal Growth Restriction and Demise through Its Anti-inflammatory Effect

Zinc Supplementation during Pregnancy Protects against Lipopolysaccharide-Induced Fetal Growth Restriction and Demise through Its Anti-inflammatory Effect

Astaxanthin Decreases Inflammatory Biomarkers Associated with Cardiovascular Disease in Human Umbilical Vein Endothelial Cells

Dynamics of PHA-induced immune response and plasma carotenoids in birds:should we have a closer look?

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