5-(4-Hydroxy-2,3,5-trimethylbenzylidene) thiazolidine-2,4-dione attenuates atherosclerosis possibly by reducing monocyte recruitment to the lesion

Choi, Jae Hoon; Park, Jong Gil; Jeon, Hyung Jun; Kim, Mi Sun; Lee, Mi Ran; Lee, Mi Ni; Sonn, Seongkeun; Kim, Jae Hong; Lee, Mun Han; Choi, Myung Sook; Park, Yong Bok; Kwon, Oh‐Seung; Jeong, Tae Sook; Lee, Woo Song; Shim, Hyun Bo; Shin, Dongkun; Oh, Goo Taeg

doi:10.3858/emm.2011.43.8.053

Cited by 14 publications

(8 citation statements)

References 30 publications

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“…Briefly, BV2 cells (5x10 5 cells/ml) were plated in 24-well plates and pre-treated with the indicated concentrations of naringenin for 1 h before treatment of 0.5 µg/ml LPS for 24 h. One hundred microliters of culture-medium supernatants were collected for determination of IL-1β, TNF-α and MCP-1 concentration by ELISA (28).…”

Section: Enzyme Immunosolvent Assay (Elisa)mentioning

confidence: 99%

Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-κB and inhibiting mitogen-activated protein kinases

Choi¹

2012

Int J Mol Med

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Abstract. Naringenin, one of the most abundant flavonoids in citrus fruits and grapefruits, has been reported to exhibit anti-inflammatory and antitumor activities. However, the cellular and molecular mechanisms underlying the naringenin anti-inflammatory activity are poorly understood. In this study, we conducted an investigation of the inhibitory effects of naringenin on the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators in BV2 microglial cells. We found that pre-treatment with naringenin prior to treatment with LPS significantly inhibited excessive production of nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) in a dose-dependent manner. The inhibition was associated with downregulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Naringenin also attenuated the production of pro-inflammatory cytokines and chemokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) by suppressing expression of mRNAs for these proteins. In addition, the molecular mechanism underlying naringenin-mediated attenuation in BV2 cells has a close relationship to suppressing translocation of the nuclear factor-κB (NF-κB) p65 subunit into the nucleus and the phosphorylation of Akt and mitogen-activated protein kinases (MAPKs). These findings suggest that naringenin may provide neuroprotection through suppression of pro-inflammatory pathways in activated BV2 microglial cells.

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Section: Enzyme Immunosolvent Assay (Elisa)mentioning

confidence: 99%

Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-κB and inhibiting mitogen-activated protein kinases

Choi¹

2012

Int J Mol Med

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“…Pharmacological inhibition of FLAP in hyperlipidemic mice did reportedly reduce atherosclerosis, although secondary effects of the drugs used cannot be excluded (315,1428). A phase II human trial with veliflapon (DG-031, DECODE Genetics) suggested modest anti-inflammatory effects (697), but a larger endpoint follow-up study was suspended without apparent explanation.…”

Section: -Lo and The Leukotrienesmentioning

confidence: 99%

Molecular Biology of Atherosclerosis

Hopkins

2013

Physiological Reviews

389

344

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At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-␣ and related family members leading to activation of NF-B; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.

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“…BHB-TZD showed anti-atherogenic effects in hyperlipidemic mice by reducing macrophage infiltration into atherosclerotic lesions, thereby increasing plaque stability (28). Another benzylidenethiazole analog, HMB-TZD, inhibits 5-lipoxygenase, reduces cell migration and adhesion by decreasing proinflammatory molecule production, and ameliorates atherosclerotic lesion formation in LDL receptor-deficient mice (29). Although increased ROS production directly causes oxidative stress in the vasculature, ROS, especially H2O2, has another important role in the pathophysiological signaling pathway of atherosclerosis.…”

Section: Figmentioning

confidence: 99%