Fructose-1,6-bisphosphate attenuates induction of nitric oxide synthase in microglia stimulated with lipopolysaccharide

Kim, Young Chae; Park, Tae Yeop; Eun-Joo, Baik; Lee, Soo Hwan

doi:10.1016/j.lfs.2011.12.011

Cited by 20 publications

(14 citation statements)

References 56 publications

(81 reference statements)

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“…These observations are in line with the previous report that FBP suppressed the activation of NF-κB in lung tissues in response to LPS challenge [45]. However, these results are not compatible with other studies where FBP did not affect LPS-mediated NF-κB activation and nuclear binding in macrophages and microglial cells [29,30]. At present, the reason for this contradiction is not clear, but it may stem from differences in the cell types expressing a specific repertoire of LPS-responsive effectors.…”

Section: Discussionsupporting

confidence: 81%

“…In this context, alternative mechanisms other than augmentation of energy metabolism have been suggested for the neuroprotective action of FBP. Those include the attenuation of oxidative stress [15,29,51,52], the antagonism of NMDA receptors [53], calcium chelation [54], the enhancement of DNA repairing ability [55] and the regulation of signaling molecules such as phospholipase C and MEK/ERK [50,52,56]. Modulation of TLR4 signaling shown in the present study could be added to the above list.…”

Section: Discussionmentioning

confidence: 99%

“…FBP alleviated carrageenan-induced pleurisy [22], suppressed T-cell proliferation [23,24] and modulated leukocyte adhesion in reperfused intestine and skeletal muscle [25,26]. In addition, it was demonstrated that FBP inhibited the production of inflammatory mediators including cytokines [24], prostaglandin E 2 [27] and advanced oxidation protein products [28] and mitigated the adverse effects of endotoxins by reducing oxidative stress and nitric oxide production [15,29,30]. These reports provide insight into the inference that anti-inflammatory effects would be implicated in the protective actions of FBP against tissue injury.…”

Section: Introductionmentioning

confidence: 99%

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Fructose-1,6-bisphosphate suppresses lipopolysaccharide-induced expression of ICAM-1 through modulation of toll-like receptor-4 signaling in brain endothelial cells

Seok

Park

et al. 2015

International Immunopharmacology

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Fructose-1,6-bisphosphate suppresses lipopolysaccharide-induced expression of ICAM-1 through modulation of toll-like receptor-4 signaling in brain endothelial cells

Seok

Park

et al. 2015

International Immunopharmacology

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“…The activation of MAPKs is also observed in LPS-stimulated microglial cells (Rayan et al 2011;Kim et al 2012). In addition, LPSinduced activation of MAPKs is implicated in the increased production of neuroinflammatory mediators such as NO, PGE 2 , and cytokines (Silva et al 1997;Murphy et al 1998;Xu and Malave 2000).…”

Section: Discussionmentioning

confidence: 90%

Suppression of LPS-induced inflammatory responses by inflexanin B in BV2 microglial cells

Lim

Sul

Hwang

et al. 2013

Can. J. Physiol. Pharmacol.

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The innate immune response is a central process that is activated during pathogenic infection in order to maintain physiological homeostasis. It is well known that dexamethasone (Dex), a synthetic glucocorticoid, is a potent immunosuppressant that inhibits the cytokine production induced by bacterial lipopolysaccharides (LPS). Nevertheless, the extent to which the functional groups of Dex control the excessive activation of inflammatory reactions remains unknown. Furthermore, importantly, the role of Dex in the innate immune response remains unclear. Here we explore the mechanism of LPS-induced TNF-α secretion and reveal p38 MAPK signaling as a target of Dex that is involved in control of tumor necrosis factor-α (TNF-α)-converting enzyme (TACE) activity; that later mediates the shedding of TNF-α that allows its secretion. We further demonstrate that the 11-hydroxyl and 21-hydroxyl groups of Dex are the main groups that are involved in reducing LPS-induced TNF-α secretion by activated macrophages. Blockage of the hydroxyl groups of Dex inhibits immunosuppressant effect of Dex during LPS-induced TNF-α secretion and mouse mortality. Our findings demonstrate Dex signaling is involved in the control of innate immunity.

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“…Multiple groups used the p47 phox dominant negative approach discussed earlier to demonstrate a specific requirement for NADPH oxidase activity in p38 and ERK phosphorylation during proinflammatory microglial activation [34, 68]. Another study with BV2 cells demonstrated that fructose-1,6-bisphosphate, a glycolytic intermediate that preserves cellular antioxidant capacity through stimulation of the pentose phosphate pathway [69], decreased LPS-induced iNOS expression to a similar extent as NAC by inhibiting JNK and p38 MAPK phosphorylation [70]. The antioxidant protein peroxiredoxin I was recently identified as an endogenous negative regulator of NF-KB-mediated microglial activation [71], providing further support for the redox-sensitivity of NF-kB.…”

Section: Mapk and Nf-kb As Hydrogen Peroxide-sensitive Regulators Of mentioning

confidence: 99%

NADPH oxidase- and mitochondria-derived reactive oxygen species in proinflammatory microglial activation: a bipartisan affair?

Bordt

Polster

2014

Free Radical Biology and Medicine

169

119

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Microglia are the resident immune cells of the brain and play major roles in central nervous system development, maintenance, and disease. Brain insults cause microglia to proliferate, migrate, and transform into one or more activated states. Classical M1 activation triggers the production of proinflammatory factors such as tumor necrosis factor- α (TNF-α), interleukin-1β (IL-1β), nitric oxide (NO), and reactive oxygen species which, in excess, can exacerbate brain injury. The mechanisms underlying microglial activation are not fully understood, yet reactive oxygen species are increasingly implicated as mediators of microglial activation. In this review, we highlight studies linking reactive oxygen species, in particular hydrogen peroxide derived from NADPH oxidase-generated superoxide, to the classical activation of microglia. In addition, we critically evaluate controversial evidence suggesting a specific role for mitochondrial reactive oxygen species in the activation of the NLRP3 inflammasome, a multiprotein complex that mediates the production of IL-1β and IL-18. Finally, the limitations of common techniques used to implicate mitochondrial ROS in microglial and inflammasome activation, such as the use of the mitochondrially-targeted ROS indicator MitoSOX and the mitochondrially-targeted antioxidant MitoTEMPO, are also discussed.

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Fructose-1,6-bisphosphate attenuates induction of nitric oxide synthase in microglia stimulated with lipopolysaccharide

Cited by 20 publications

References 56 publications

Fructose-1,6-bisphosphate suppresses lipopolysaccharide-induced expression of ICAM-1 through modulation of toll-like receptor-4 signaling in brain endothelial cells

Fructose-1,6-bisphosphate suppresses lipopolysaccharide-induced expression of ICAM-1 through modulation of toll-like receptor-4 signaling in brain endothelial cells

Suppression of LPS-induced inflammatory responses by inflexanin B in BV2 microglial cells

NADPH oxidase- and mitochondria-derived reactive oxygen species in proinflammatory microglial activation: a bipartisan affair?

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