Anti-inflammatory effects of trans-cinnamaldehyde on lipopolysaccharide-stimulated macrophage activation via MAPKs pathway regulation

Kim, Mi Eun; Na, Ju Yong; Lee, Jun Sik

doi:10.1080/08923973.2018.1424902

Cited by 66 publications

(40 citation statements)

References 30 publications

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“…Herein, it was found that cinnamaldehyde reduces the production of key inflammatory mediators (IL-17, VEGF and NO) in the wound beds of P. aeruginosa -infected mice. Cinnamaldehyde anti-inflammatory effects are not novel, and different studies have demonstrated its ability to reduce NO and pro-inflammatory cytokine generation upon LPS stimuli [26,35,36,37]. However, its modulatory role on VEGF expression is unclear.…”

Section: Discussionmentioning

confidence: 99%

Topical Application of Cinnamaldehyde Promotes Faster Healing of Skin Wounds Infected with Pseudomonas aeruginosa

Ferro¹,

Souza²,

Suarez³

et al. 2019

Molecules

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Wound healing can be delayed following colonization and infection with the common bacterium Pseudomonas aeruginosa. While multiple therapies are used for their treatment, these are ineffective, expensive, and labour-intensive. Thus, there is an enormous unmet need for the treatment of infected wounds. Cinnamaldehyde, the major component of cinnamon oil, is well known for its antimicrobial properties. Herein, we investigated the effects of sub-inhibitory concentrations of cinnamaldehyde in the virulence of P. aeruginosa. We also assessed its healing potential in P. aeruginosa-infected mouse skin wounds and the mechanisms involved in this response. Sub-inhibitory concentrations of cinnamaldehyde reduced P. aeruginosa metabolic rate and its ability to form biofilm and to cause haemolysis. Daily topical application of cinnamaldehyde on P. aeruginosa-infected skin wounds reduced tissue bacterial load and promoted faster healing. Lower interleukin-17 (IL-17), vascular endothelial growth factor (VEGF) and nitric oxide levels were detected in cinnamaldehyde-treated wound samples. Blockage of transient receptor potential ankyrin 1, the pharmacological target of cinnamaldehyde, abrogated its healing activity and partially reversed the inhibitory actions of this compound on VEGF and IL-17 generation. We suggest that topical application of sub-inhibitory concentrations of cinnamaldehyde may represent an interesting approach to improve the healing of P. aeruginosa-infected skin wounds.

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Section: Discussionmentioning

confidence: 99%

Topical Application of Cinnamaldehyde Promotes Faster Healing of Skin Wounds Infected with Pseudomonas aeruginosa

Ferro¹,

Souza²,

Suarez³

et al. 2019

Molecules

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“…It has been reported that TCA has anti-inflammatory effects [13, 16, 35], such as inhibiting the expression of inflammatory factors like IL-1 β , NO, and PGE 2 [13, 15, 35]. Nevertheless, whether TCA has benefits against cartilage degradation in OA-like inflammation is still unknown.…”

Section: Discussionmentioning

confidence: 99%

“…However, he chose to exam kidney instead of cartilage because he believed it is vulnerable to oxidative stress and inflammation stimuli. Recently, the anti-inflammatory effects of TCA in LPS-induced macrophages produced via the suppression of mitogen-activated protein kinase (MAPKs) phosphorylation and proinflammatory genes were also revealed [35].…”

Section: Discussionmentioning

confidence: 99%

Trans-Cinnamaldehyde Inhibits IL-1β-Stimulated Inflammation in Chondrocytes by Suppressing NF-κB and p38-JNK Pathways and Exerts Chondrocyte Protective Effects in a Rat Model of Osteoarthritis

Xia

Gao

Zhou

et al. 2019

BioMed Research International

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Objective. Trans-cinnamaldehyde (TCA), a compound from Cinnamomum cassia Presl, has been reported to have anti-inflammatory effect. However, its effect on cartilage degradation in osteoarthritis is unclear. This study is designed to examine the effects of TCA on cartilage in vitro and in vivo. Material and Methods. SW1353 cells and human primary chondrocytes were treated with varying concentrations of TCA (2-20 μg/ml) for 2 h followed by IL-1β stimulation. Cell viability was examined by the MTT assay. Expression of MMP-1, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5 was examined by Western blot and RT-qPCR. Monosodium iodoacetate (MIA)-induced OA was established in rats to assess the chondrocyte protective effects of intraperitoneal injection of TCA (50 mg/kg). Results. TCA at a concentration of 10 μg/ml had no significant effect on cell viability. MMP-1, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5 were decreased by TCA 2-10 μg/ml in a dose-dependent manner (all P<0.05). Pretreatment with TCA decreased the degradation of IκBα and increased the expression of p-IκBα, indicating that NF-κB inactivation was induced by TCA in IL-1β-stimulated SW1353 cells. Pretreatment with TCA decreased the levels of p-p38 and p-JNK, while the levels of p-ERK were not significantly affected. TCA 10 μg/ml significantly decreased expression levels of MMP-1, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5. In vivo results showed that TCA alleviated cartilage destruction and the OARSI scores. Conclusion. TCA possesses anti-inflammatory effect in vitro and exerts chondrocyte protective effects in vivo, in which NF-κB and p38-JNK were involved.

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“…Cinnamaldehyde, but not cinnamic acid, cinnamic alcohol and coumarin, inhibits the production of NO, TNFα and PGE2 by LPS-stimulated RAW264.7 cells (1). Cinnamaldehyde was also reported to inhibit the inflammatory activity of LPS-stimulated macrophages via suppression of mitogen-activated protein kinase (MAPK) phosphorylation and pro-inflammatory gene expression (67). Furthermore, it has been reported that when RAW264.7 macrophages were treated with cinnamaldehyde together with E. coli LPS, significant concentration-dependent inhibition of NO, TNFα, and PGE2 production was detected (1).…”

Section: Stimulation Of Ho1 Mrna Expression By Cinnamates and (Meth)amentioning

confidence: 99%

Cytotoxicity and Pro-/Anti-inflammatory Properties of Cinnamates, Acrylates and Methacrylates Against RAW264.7 Cells

Murakami

Kawata

Suzuki

et al. 2018

In Vivo

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Background/Aim: Periodontitis is a chronic inflammatory disease linked to various systemic age-related conditions. It is known that α,β-unsaturated carbonyl compounds such as dietary cinnamates (β-phenyl acrylates) and related (meth)acrylates can have various positive and negative health effects, including cytotoxicity, allergic activity, pro-and anti-inflammatory activity, and anticancer activity. To clarify the anti-inflammatory properties of α,β-unsaturated carbonyl compounds without a phenolic group in the context of periodontal tissue inflammation and alveolar bone loss, we investigated the cytotoxicity and up-regulatory/downregulatory effect of three trans-cinnamates (trans-cinnamic acid, methyl cinnamate, trans-cinnamaldehyde), two acrylates (ethyl acrylate, 2-hydroxyethyl acrylate), and three methacrylates (methyl methacrylate, 2-hydroxyethyl methacrylate, and triethyleneglycol dimethacrylate) using RAW264.7 cells. Materials and Methods: Cytotoxicity was determined using a cell counting kit (CCK-8) and mRNA expression was determined using real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Proinflammatory and anti-inflammatory properties were assessed in terms of expression of mRNAs for cyclo-oxygenase-2 (Cox2), nitric oxide synthase 2 (Nos2), tumor necrosis factoralpha (Tnfa) and heme oxygenase 1 (Ho1). Results: The most cytotoxic compound was 2-hydroxyethyl acrylate, followed by ethyl acrylate and cinnamaldehyde (50% lethal cytotoxic concentration, LC 50 =0.2-0.5 mM). Cox2 mRNA expression was up-regulated by cinnamaldehyde and 2-hydroxyethyl acrylate, particularly by the former. In contrast, the upregulatory effect on Nos2 mRNA expression was in the order: cinnamaldehyde >> ethyl acrylate ≈ triethyleneglycol dimethacrylate >> methyl methacrylate ≈ methyl cinnamate. On the other hand, cinnamic acid and 2-hydroxyethyl methacrylate had no effect on gene expression. The two acrylates, but not cinnamates and methacrylates, up-regulated the expression of Ho1 mRNA at a non-cytotoxic concentration of 0.1 mM. Expression of Cox2, Nos2 and Tnfa mRNAs induced by Porphyromonas gingivalis lipopolysaccharide was greatly suppressed by cinnamaldehyde, methyl cinnamate and the two acrylates at 0.1 mM (p<0.05), and slightly, but significantly suppressed by cinnamic acid and methacrylates at 0.

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Anti-inflammatory effects of trans-cinnamaldehyde on lipopolysaccharide-stimulated macrophage activation via MAPKs pathway regulation

Cited by 66 publications

References 30 publications

Topical Application of Cinnamaldehyde Promotes Faster Healing of Skin Wounds Infected with Pseudomonas aeruginosa

Topical Application of Cinnamaldehyde Promotes Faster Healing of Skin Wounds Infected with Pseudomonas aeruginosa

Trans-Cinnamaldehyde Inhibits IL-1β-Stimulated Inflammation in Chondrocytes by Suppressing NF-κB and p38-JNK Pathways and Exerts Chondrocyte Protective Effects in a Rat Model of Osteoarthritis

Cytotoxicity and Pro-/Anti-inflammatory Properties of Cinnamates, Acrylates and Methacrylates Against RAW264.7 Cells

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