Cinnamaldehyde inhibits pro-inflammatory cytokines secretion from monocytes/macrophages through suppression of intracellular signaling

Chao, Louis Kuoping; Hua, Kuo-Feng; Hsu, Han‐Shui; Cheng, Sen‐Sung; Lin, I‐Fan; Chen, Chia‐Jung; Chen, Shui‐Tein; Chang, Shang‐Tzen

doi:10.1016/j.fct.2007.07.016

Cited by 203 publications

(156 citation statements)

References 45 publications

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“…Roth-Walter and Moskovskich et al showed that CA exhibits immune suppressive effects by inhibiting proliferation and inducing apoptosis in primary immune cell lines even at 10 μM [34]. Furthermore, CA has been shown to inhibit secretion of pro-inflammatory cytokines [35] while promoting anti-inflammatory cytokine release [36] from macrophages in vitro . In our balloon injured ZDF carotid arteries we saw reduced presence of both neutrophils and macrophages and the aforementioned anti-inflammatory properties of CA may have contributed to this reduction in inflammatory cell number.…”

Section: Discussionmentioning

confidence: 99%

Cinnamic aldehyde inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia in Zucker Diabetic Fatty rats

2018

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Atherosclerosis remains the number one cause of death and disability worldwide. Atherosclerosis is treated by revascularization procedures to restore blood flow to distal tissue, but these procedures often fail due to restenosis secondary to neointimal hyperplasia. Diabetes mellitus is a metabolic disorder that accelerates both atherosclerosis development and onset of restenosis. Strategies to inhibit restenosis aim at reducing neointimal hyperplasia by inhibiting vascular smooth muscle cell (VSMC) proliferation and migration. Since increased production of reactive oxygen species promotes VSMC proliferation and migration, redox intervention to maintain vascular wall redox homeostasis holds the potential to inhibit arterial restenosis. Cinnamic aldehyde (CA) is an electrophilic Nrf2 activator that has shown therapeutic promise in diabetic rodent models. Nrf2 is a transcription factor that regulates the antioxidant response. Therefore, we hypothesized that CA would activate Nrf2 and would inhibit neointimal hyperplasia after carotid artery balloon injury in the Zucker Diabetic Fatty (ZDF) rat. In primary ZDF VSMC, CA inhibited cell growth by MTT with an EC50 of 118 ± 7 μM. At a therapeutic dose of 100 μM, CA inhibited proliferation of ZDF VSMC in vitro and reduced the proliferative index within the injured artery in vivo, as well as migration of ZDF VSMC in vitro. CA activated the Nrf2 pathway in both ZDF VSMC and injured carotid arteries while also increasing antioxidant defenses and reducing markers of redox dysfunction. Additionally, we noted a significant reduction of neutrophils (69%) and macrophages (78%) within the injured carotid arteries after CA treatment. Lastly, CA inhibited neointimal hyperplasia evidenced by a 53% reduction in the intima:media ratio and a 61% reduction in vessel occlusion compared to arteries treated with vehicle alone. Overall CA was capable of activating Nrf2, and inhibiting neointimal hyperplasia after balloon injury in a rat model of diabetic restenosis.

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Section: Discussionmentioning

confidence: 99%

Cinnamic aldehyde inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia in Zucker Diabetic Fatty rats

2018

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“…Thymol scavenges reactive oxygen species (ROS) in neutrophils (Braga et al, 2006). Cinnamaldehyde inhibits ROS production (Chao et al, 2008) to impede NF-κB activation (Youn et al, 2008), consequently suppressing proinflammatory targets, such as cytokines, and LPSinduced COX2 gene expression (Chao et al, 2008;Youn et al, 2008). In connection with the lack of supression of COX2 gene expression in Caco-2 cells in physiological state, the experiment with LPS-induced COX2 gene expression prior to EO treatment needs to be conducted in the future.…”

Section: Discussionmentioning

confidence: 99%

Effects of cinnamaldehyde and thymol on cytotoxicity, tight junction barrier resistance, and cyclooxygenase-1 and -2 expression in Caco-2 cells

Putaala¹,

Nurminen²,

Tiihonen³

2017

J. Anim. Feed Sci.

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“…To verify the mechanism of action underlying the anti-inflammatory effects of C. obtusa essential oil, we also examined the regulation of COX-2 expression levels. Pathogen-associated immune responses are antigenic, and are able to activate monocytes or macrophages to synthesize various inflammatory cytokines, including IL-1, IL-6 and TNF, which have been reported to be mediated via COX expression (24)(25)(26). The expression of COX-2 was increased following treatment with LPS, and this upregulation was inhibited by C. obtusa essential oil in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of essential oils from Chamaecyparis obtusa via the cyclooxygenase-2 pathway in rats

Kang

Yang

et al. 2013

Molecular Medicine Reports

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Abstract. Essential oils are concentrated hydrophobic liquids containing volatile aromatic compounds from plants. In the present study, the essential oil of Chamaecyparis obtusa (C. obtusa), which is commercially used in soap, toothpaste and cosmetics, was extracted. Essential oil extracted from C. obtusa contains several types of terpenes, which have been shown to have anti-oxidative and anti-inflammatory effects. In the present study, we examined the anti-inflammatory effects of C. obtusa essential oil in vivo and in vitro following the induction of inflammation by lipopolysaccharides (LPS) in rats. While LPS induced an inflammatory response through the production of prostaglandin E 2 (PGE 2 ) in the blood and peripheral blood mononuclear cells (PMNCs), these levels were reduced when essential oil was pre-administered. Additionally, the mechanism of action underlying the anti-inflammatory effects of C. obtusa essential oil was investigated by measuring the mRNA expression of inflammation-associated genes. LPS treatment significantly induced the expression of transforming growth factor α (TNFα) and cyclooxygenase-2 (COX-2) in rats, while C. obtusa essential oil inhibited this effect. Taken together, our results demonstrate that C. obtusa essential oil exerts anti-inflammatory effects by regulating the production of PGE 2 and TNFα gene expression through the COX-2 pathway. These findings suggest that C. obtusa essential oil may constitute a novel source of anti-inflammatory drugs.

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Cinnamaldehyde inhibits pro-inflammatory cytokines secretion from monocytes/macrophages through suppression of intracellular signaling

Cited by 203 publications

References 45 publications

Cinnamic aldehyde inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia in Zucker Diabetic Fatty rats

Cinnamic aldehyde inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia in Zucker Diabetic Fatty rats

Effects of cinnamaldehyde and thymol on cytotoxicity, tight junction barrier resistance, and cyclooxygenase-1 and -2 expression in Caco-2 cells

Anti-inflammatory effects of essential oils from Chamaecyparis obtusa via the cyclooxygenase-2 pathway in rats

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