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cinnamaldehyde/φλεγμονή
Ο σύνδεσμος αποθηκεύεται στο πρόχειρο
Σελίδα 1 από 213 Αποτελέσματα
The involvement of TRPA1 channel activation in the inflammatory response evoked by topical application of cinnamaldehyde to mice.
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OBJECTIVE
In the present work, we characterize the inflammatory process induced by the topical application of cinnamaldehyde on the skin of mice and verify the participation of transient receptor potential A1 TRPA1 receptors in this process.
METHODS
We measured mouse ear edema and
Submicron emulsion of cinnamaldehyde ameliorates bleomycin-induced idiopathic pulmonary fibrosis via inhibition of inflammation, oxidative stress and epithelial-mesenchymal transition.
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OBJECTIVE
Idiopathic pulmonary fibrosis (IPF) is the most frequent and severe form of idiopathic interstitial pneumonias. The pathogenesis is associated with inflammation and oxidative stress and epithelial-mesenchymal transition (EMT). Cinnamaldehyde exhibits antiinflammatory and antioxidant
Anti-inflammatory effects of trans-cinnamaldehyde on lipopolysaccharide-stimulated macrophage activation via MAPKs pathway regulation.
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OBJECTIVE
Inflammation is a primary response of the innate immune system against various infections. Macrophages are a type of immune cell that have a critical role in the inflammation. Recent studies reported that various natural compounds could regulate immune responses such as inflammation.
Preparation of a calcium carbonate-based bone substitute with cinnamaldehyde crosslinking agent with potential anti-inflammatory properties.
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Calcium sulfate (CS), also known as POP (Plaster of Paris) is a self-setting, biocompatible, and osteoconductive biomaterial with a long history for the treatment of skeletal defects. However, CS cements show a too fast resorption rate and are unable to provide a long-term 3D framework during the
Suppression of age-related inflammatory NF-kappaB activation by cinnamaldehyde.
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Redox sensitive, pro-inflammatory nuclear transcription factor NF-kappaB plays a key role in both inflammation and aging processes. In a redox state disrupted by oxidative stress, pro-inflammatory genes are upregulated by the activation of NF-kappaB through diverse kinases. Thus, the search and
[Cinnamaldehyde attenuates lipopolysaccharide induced inflammation and apoptosis in human umbilical vein endothelial cells].
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Objective: To investigate the effect of cinnamaldehyde (CIN) on the inflammation and apoptosis on human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS), and to explore the potential mechanisms. Methods: HUVECs were divided in to 8 groups: blank control
Anti-oxidative and anti-inflammatory effects of cinnamaldehyde on protecting high glucose-induced damage in cultured dorsal root ganglion neurons of rats.
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OBJECTIVE
To examine the mechanism underlying the beneficial role of cinnamaldehyde on oxidative damage and apoptosis in high glucose (HG)-induced dorsal root ganglion (DRG) neurons in vitro.
METHODS
HG-treated DRG neurons were developed as an in vitro model of diabetic neuropathy. The neurons were
Cinnamaldehyde derivatives inhibit degranulation and inflammatory mediator production in rat basophilic leukemia cells.
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Mast cells play a critical role in allergic diseases. Therefore, development of new therapeutic agents that suppresses the activation of mast cells may help prevent or treat allergic diseases. Here, we investigated the anti-allergic effects of 4-chloro-cinnamaldehyde and 4-trifluoro-cinnamaldehyde
Cinnamaldehyde is an effective anti-inflammatory agent for treatment of allergic rhinitis in a rat model.
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OBJECTIVE
The effect of cinnamaldehyde on the treatment of allergic rhinitis (AR) was investigated in rat model.
METHODS
Twenty-eight female Wistar albino rats were randomly divided into four groups: Group 1 (control) (C), Group 2 (AR with no treatment) (AR+NoTr), Group 3 (AR+Azelastine HCl)
Cinnamaldehyde protects against oxidative stress and inhibits the TNF‑α‑induced inflammatory response in human umbilical vein endothelial cells.
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Oxidative stress and inflammation play critical roles in the development of cardiovascular diseases. Cinnamaldehyde (CA) is a natural compound from Cinnamomum cassia, and its anticancer, antimicrobial and anti‑inflammatory activities have been widely investigated. In the present study, the
Cinnamaldehyde modulates LPS-induced systemic inflammatory response syndrome through TRPA1-dependent and independent mechanisms.
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Cinnamaldehyde is a natural essential oil suggested to possess anti-bacterial and anti-inflammatory properties; and to activate transient receptor potential ankyrin 1 (TRPA1) channels expressed on neuronal and non-neuronal cells. Here, we investigated the immunomodulatory effects of cinnamaldehyde
Cinnamaldehyde inhibits inflammation of human synoviocyte cells through regulation of Jak/Stat pathway and ameliorates collagen-induced arthritis in rats.
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Cinnamaldehyde (Cin), a bioactive cinnamon essential oil from traditional Chinese medicine (TCM) herb Cinnamomum cassia, has been reported to have multi-pharmacological activities including anti-inflammation. However, its role and molecular mechanism of anti-inflammatory activity in musculoskeletal
Anti-inflammatory activity of cinnamon (C. zeylanicum and C. cassia) extracts - identification of E-cinnamaldehyde and o-methoxy cinnamaldehyde as the most potent bioactive compounds.
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Chronic inflammation is a contributing factor in many age-related diseases. In a previous study, we have shown that Sri Lankan cinnamon (C. zeylanicum) was one of the most potent anti-inflammatory foods out of 115 foods tested. However, knowledge about the exact nature of the anti-inflammatory
Regulatory effect of cinnamaldehyde on monocyte/macrophage-mediated inflammatory responses.
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Cinnamaldehyde (CA) has been known to exhibit anti-inflammatory and anticancer effects. Although numerous pharmacological effects have been demonstrated, regulatory effect of CA on the functional activation of monocytes and macrophages has not been fully elucidated yet. To evaluate its
Cinnamaldehyde and eugenol attenuates collagen induced arthritis via reduction of free radicals and pro-inflammatory cytokines.
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