Anti-oxidant and anti-inflammatory effects of cinnamaldehyde and eugenol on mononuclear cells of rheumatoid arthritis patients

Mateen, Somaiya; Rehman, Tabish; Shahzad, Sumayya; Naeem, Syed Shariq; Faizy, Abul Faiz; Khan, Abdul Qayyum; Khan, Mohd Shahnawaz; Husain, Fohad Mabood; Moin, Shagufta

doi:10.1016/j.ejphar.2019.02.031

Cited by 96 publications

(59 citation statements)

References 57 publications

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“…Treatment with cinnamaldehyde significantly reduced serum RF and the pro-inflammatory cytokines IL-6 and TNF-α, while elevated the anti-inflammatory cytokine IL-10. Our results were consistent with those of previous studies, where cinnamaldehyde has been reported to reduce IL-6 and TNF-α when administered to collagen treated rats ( Mateen et al, 2019a , Mateen et al, 2019b ), added to blood cell culture from RA patients ( Mateen et al, 2019a , Mateen et al, 2019b ), and J774A.1 cells stimulated by lipopolysaccharide resulting also in the enhancement of IL-10 production ( Pannee et al, 2014 ). Additionally, treatment with cinnamaldehyde reduced serum RANKL and MMP-3, along with suppression of JAK2/STAT3 signaling that explored the molecular mechanism of cinnamaldehyde in reducing cartilage and bone erosion in RA.…”

Section: Discussionsupporting

confidence: 93%

“…Cinnamaldehyde is a potent anti-inflammatory constituent of cinnamon essential oil ( Gunawardena et al, 2015 ). It has been previously reported to alleviate arthritis induced by collagen through regulation of oxidative stress and inflammatory markers ( Mateen et al, 2019a , Mateen et al, 2019b ), and to suppress JAK/STAT signaling in synoviocytes ( Cheng et al, 2020 ), but its effect on joint destruction biomarkers hasn't been investigated before.…”

Section: Introductionmentioning

confidence: 99%

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Aliskiren, tadalafil, and cinnamaldehyde alleviate joint destruction biomarkers; MMP-3 and RANKL; in complete Freund's adjuvant arthritis model: Downregulation of IL-6/JAK2/STAT3 signaling pathway

Azouz

Saleh

Abo-Saif

2020

Saudi Pharmaceutical Journal

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Rheumatoid arthritis (RA) is an autoimmune inflammatory disease, which is accompanied by progressive joint damage and disability. The intolerability of conventional antirheumatic drugs by some patients necessitates the search for effective antirheumatic agents having better tolerability. In the current work, we aimed to investigate the efficacy of cinnamaldehyde, tadalafil, and aliskiren as potential antirheumatic candidates and to explore their modulatory effects on joint destruction, inflammatory response, and intracellular signaling. Arthritis was induced in female Wistar rats by complete Freund's adjuvant (CFA) 0.4 ml s.c. on days 1, 4, and 7. Treated groups received their respective drugs, starting from day 13, daily for 3 weeks. Methotrexate and prednisolone were the standard antirheumatic drugs, while cinnamaldehyde, tadalafil, and aliskiren were the test agents. Treatment with cinnamaldehyde, tadalafil, or aliskiren reduced serum levels of rheumatoid factor, and pro-inflammatory cytokines; tumor necrosis factor-alpha and interleukin-6 (IL-6), along with elevated level of IL-10 which is an anti-inflammatory cytokine. Besides, cartilage and bone destruction biomarkers; matrix metalloproteinase-3 (MMP-3) and receptor activator of nuclear factor-kappa B ligand (RANKL); were significantly reduced after treatment with the test agents, which was further confirmed by histopathological investigation. The elevated protein expressions of phosphorylated-Janus kinase 2 (p-JAK2), phosphorylated-signal transducer and activator of transcription 3 (p-STAT3), and inducible nitric oxide synthase (iNOS) in articular tissue were markedly attenuated after treatment with cinnamaldehyde, tadalafil, or aliskiren, while that of endothelial nitric oxide synthase (eNOS) was greatly enhanced. In addition, oxidative stress and inflammatory markers such as malondialdehyde, nitric oxide, and myeloperoxidase were reduced in joint tissue after treatment with the test agents, while glutathione content was elevated. Furthermore, the renin inhibitor aliskiren produced effects close to those of the normal and methotrexate, the gold standard antirheumatic drug, in most of the measured parameters. Collectively, these findings led to the assumption that the downregulation of IL-6/JAK2/STAT3 signaling by cinnamaldehyde, tadalafil, and aliskiren could alleviate joint destruction by MMP-3 and RANKL, reduce iNOS, and enhance eNOS expressions. Moreover, aliskiren could be a promising therapeutic agent for RA, because of its ability to normalize most of the measured parameters after CFA-induced arthritis.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Aliskiren, tadalafil, and cinnamaldehyde alleviate joint destruction biomarkers; MMP-3 and RANKL; in complete Freund's adjuvant arthritis model: Downregulation of IL-6/JAK2/STAT3 signaling pathway

Azouz

Saleh

Abo-Saif

2020

Saudi Pharmaceutical Journal

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“…Furthermore, oxidative stress caused by reactive oxygen species (ROS) is crucial in joint in ammation, and RA patients exhibit high level of ROS in serum [18,19]. Hence, antioxidant drugs may be effective in treating RA [20]. Collagen-induced arthritis (CIA) in mice recapitulates the clinical and pathogenic characteristics of human RA, and are widely used to study RA [21].…”

Section: Introductionmentioning

confidence: 99%

Aqueous extract of Kan-Lu-Hsiao-Tu-Tan ameliorates collagen-induced arthritis in mice by regulating immune and inflammatory responses

Chiang

Lai

et al. 2020

Preprint

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Background: Kan-Lu-Hsiao-Tu-Tan (KLHTT) exhibits anti-psoriatic effects through anti-inflammatory activity in mice. However, the therapeutic effects of KLHTT on rheumatoid arthritis (RA), another significant autoimmune inflammatory disorder, are not elucidated. Herein, we explored the anti-arthritic effects of KLHTT on collagen-induced arthritis (CIA) in mice. Methods: KLHTT was extracted by boiling water and subjected to spectroscopic analysis. Chicken collagen type II (CII) with complete Freund’s adjuvant was intradermally injected to induce CIA in DBA/1J mice. Anti-CII antibody, cytokines, malondialdehyde (MDA), and hydrogen peroxide (H2O2) were measured using ELISA, thiobarbituric acid reactive substances, and hydrogen peroxide assay kit. Splenocyte proliferation was tested using thymidine incorporation. Th1 and Th17 cells were analyzed by flow cytometry. Results: Oral KLHTT treatment (50 and 100 mg/kg) ameliorated mouse CIA by decreasing the levels of interleukin (IL)-1β, IL-6, IL-17A, and tumour necrosis factor-α in the paw homogenates and serum. KLHTT also suppressed anti-CII antibody formation, splenocyte proliferation, and splenic Th1 and Th17 cell numbers. Additionally, KLHTT showed antioxidant activity by reducing the concentrations of MDA and H2O2 in paw tissues. Conclusions: The therapeutic effects of KLHTT in CIA mice were through regulating oxidative stress and inflammatory responses. Our results suggest that KLHTT has potential to treat RA.

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“…This compound is generally recognized as safe (GRAS) by the United States Food and Drug Administration (FDA), and Flavour and Extract Manufacturer's Association (FEMA), and has been granted A status (may be used in foodstuffs) by the Council of Europe [15][16][17].Cinnamaldehyde is active against pathogenic bacteria, fungi, and viruses [18], besides other activities related to human health like antiinflammatory, and antioxidant potentials. Therefore, it is widely used in the food, drug, and cosmetic industries [19]. However, EOs and their individual constituents are generally unstable in the presence of light, heat, oxygen, and humidity.…”

Section: Introductionmentioning

confidence: 99%

Eco-Friendly Cinnamaldehyde Based Emulsion for Phytopathogenic Bacterial Growth Inhibitor

Mohammed

El-Rahman

2020

JAMB

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The formulation plays an essential role in achieving the successful delivery and biological activity of any plant protection products. This study aimed to develop a cinnamaldehyde water-based formulation (oil-in-water emulsion) via a high-shear stirring emulsification method. Cinnamaldehyde emulsion was successfully prepared and characterized using different physicochemical parameters (emulsion stability, persistent foaming, accelerated storage at 54°C for 2 weeks, and stability at 0°Cfor one week, as well as pH, surface tension, flash point, viscosity, and particle size distribution). Also, the antibacterial activity was verified in vitro against some important phytopathogenic bacteria; Erwinia amylovora, Pectobacterium aroidearum, Pseudomonas aeruginosa, and Ralstonia solanacearum using well diffusion method. In addition, the minimum inhibition concentration (MIC) was determined by the twofold dilution method. The results revealed that the prepared formulation showed good storage stability, exhibited non-Newtonian shear-thinning behavior and promising antibacterial activity. The inhibition zones against the tested phytopathogenic bacteria were ranged from 10.3 mm to 52.0 mm. MICs of the prepared formulation were 15.63, 31.25, 62.5, and 15.63 μl/ml against Erwinia amylovora, Pectobacterium aroidearum, Pseudomonas aeruginosa and Ralstonia solanacearum, respectively. Our results provide an environmentally friendly formulation with promising activity to control the agricultural crop disease.

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Anti-oxidant and anti-inflammatory effects of cinnamaldehyde and eugenol on mononuclear cells of rheumatoid arthritis patients

Cited by 96 publications

References 57 publications

Aliskiren, tadalafil, and cinnamaldehyde alleviate joint destruction biomarkers; MMP-3 and RANKL; in complete Freund's adjuvant arthritis model: Downregulation of IL-6/JAK2/STAT3 signaling pathway

Aliskiren, tadalafil, and cinnamaldehyde alleviate joint destruction biomarkers; MMP-3 and RANKL; in complete Freund's adjuvant arthritis model: Downregulation of IL-6/JAK2/STAT3 signaling pathway

Aqueous extract of Kan-Lu-Hsiao-Tu-Tan ameliorates collagen-induced arthritis in mice by regulating immune and inflammatory responses

Eco-Friendly Cinnamaldehyde Based Emulsion for Phytopathogenic Bacterial Growth Inhibitor

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