Rutin Attenuates Oxidative Stress and Proinflammatory Cytokine Level in Adjuvant Induced Rheumatoid Arthritis via Inhibition of NF-&amp;#x03BA;B

Sun, Chaoyang; Wei, Jun; Bi, Liqi

doi:10.1159/000451027

Cited by 42 publications

(18 citation statements)

References 21 publications

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“…Among them, p50 and p65 are the most relevant subunits to RA synoviocytes by immunohistochemistry [ 5 ]. Prior studies showed that suppression of NF-κB p65, the main effector subunit of the classical NF-κB pathway, protects against RA [ 36 ]. The transcriptional activity of p65 could be further regulated by phosphorylation and acetylation.…”

Section: Discussionmentioning

confidence: 99%

SIRT1 inhibits rheumatoid arthritis fibroblast-like synoviocyte aggressiveness and inflammatory response via suppressing NF-κB pathway

Xia

Liu

et al. 2018

Bioscience Reports

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Rheumatoid arthritis (RA) is an autoimmune disease of the joints characterized by synovial hyperplasia and chronic inflammation. Fibroblast-like synoviocytes (FLS) play a central role in RA initiation, progression, and perpetuation. Prior studies showed that sirtuin 1 (SIRT1), a deacetylase participating in a broad range of transcriptional and metabolic regulations, may impact cell proliferation and inflammatory responses. However, the role of SIRT1 in RA–FLS was unclear. Here, we explored the effects of SIRT1 on the aggressiveness and inflammatory responses of cultured RA-FLS. SIRT1 expression was significantly lower in synovial tissues and FLS from RA patients than from healthy controls. Overexpression of SIRT1 significantly inhibited RA-FLS proliferation, migration, and invasion. SIRT1 overexpression also significantly increased RA-FLS apoptosis and caspase-3 and -8 activity. Focusing on inflammatory phenotypes, we found SIRT1 significantly reduced RA-FLS secretion of TNF-α, IL-6, IL-8, and IL-1β. Mechanistic studies further revealed SIRT1 suppressed NF-κB pathway by reducing p65 protein expression, phosphorylation, and acetylation in RA-FLS. Our results suggest SIRT1 is a key regulator in RA pathogenesis by suppressing aggressive phenotypes and inflammatory response of FLS. Enhancing SIRT1 expression or function in FLS could be therapeutic beneficial for RA by inhibiting synovial hyperplasia and inflammation.

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Section: Discussionmentioning

confidence: 99%

SIRT1 inhibits rheumatoid arthritis fibroblast-like synoviocyte aggressiveness and inflammatory response via suppressing NF-κB pathway

Xia

Liu

et al. 2018

Bioscience Reports

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“…In addition, histopathological examination showed that the inflammatory cells infiltration, synovial hyperplasia, pannus formation and cartilage and bone erosion had considerably improved on administration of rutin. Thus, these findings demonstrated the protective effect of rutin against rheumatoid arthritis via suppression of NF-κB p65 protein expression (Sun et al, 2017).…”

Section: Antiarthritis Propertymentioning

confidence: 64%

A review on the chemistry and biological properties of Rutin, a promising nutraceutical agent

Prasad¹,

Prasad²

2019

Asian J Pharm Pharmacol

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Nature is an attractive source of new therapeutic agents and a variety of phytochemicals have proved to be very valuable in the prevention and treatment of various diseases. Many of the important drugs isolated from plants during the past 50 years have revolutionized modern medicinal practice (Dar et al., 2017). The use of herbal medicines and phytonutrients or nutraceuticals continues to expand rapidly across the world with many people now resorting to these products for the treatment of various health challenges in different national healthcare settings (WHO, 2004). It is estimated that up to 80% of the world's population living in the developing countries rely on herbal medicinal products as a primary source of healthcare and traditional medical practice as an integral part of the culture in their communities (Ekor, 2013). The medicinal compounds derived from various plants could be divided into three major biochemical classes: alkaloids (vinblastine, vincristine, pilocarpine, berberine, caffeine, piperine etc.), flavonoids (quercetin, kaempferol, chrysin, naringenin, genistein, rutin etc.) and terpenoids (artemisinin, taxol, digitoxin, azadarachtin, camphor, limonene etc.) (Takshak, 2018). These compounds have also gained importance in the area of nutraceuticals, which have positive health effects and may prove to be advantageous in the treatment of diseases like cancer, cardiovascular diseases and diabetes (Crozier et

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“…Our investigations also explored that CFA-induced arthritis elevated MDA, and reduced GSH contents in the articular tissue. Similarly, different studies have demonstrated oxidant/antioxidant imbalance after CFA-induced arthritis ( Liu et al, 2017 , Sun et al, 2017 ).…”

Section: Discussionmentioning

confidence: 90%

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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Rutin Attenuates Oxidative Stress and Proinflammatory Cytokine Level in Adjuvant Induced Rheumatoid Arthritis via Inhibition of NF-κB

Cited by 42 publications

References 21 publications

SIRT1 inhibits rheumatoid arthritis fibroblast-like synoviocyte aggressiveness and inflammatory response via suppressing NF-κB pathway

SIRT1 inhibits rheumatoid arthritis fibroblast-like synoviocyte aggressiveness and inflammatory response via suppressing NF-κB pathway

A review on the chemistry and biological properties of Rutin, a promising nutraceutical agent

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

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