Association of oxidative stress with clinical characteristics in patients with rheumatoid arthritis

Kardeş, Sinan; Karagülle, Mine; Durak, İlker; Avcı, Aslıhan

doi:10.1111/eci.12858

Cited by 13 publications

(13 citation statements)

References 46 publications

(149 reference statements)

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“…Over the past several decades, oxidative stress has been found to be involved in the pathogenesis and development of many diseases, including ophthalmic diseases (Nishimura et al, 2017;Pinazo-Duran et al, 2018), diabetes (Rochette et al, 2018), cardiovascular diseases (Luscher, 2015;Munzel et al, 2015;Schiattarella and Hill, 2017), atherosclerosis (Forstermann et al, 2017), arthritis (Bala et al, 2017;Kardes and Karagulle, 2018), dermatological diseases (Rojo de la Vega et al, 2018), respiratory diseases (Hecker, 2018), hepatic diseases (Lee et al, 2019), urinary system diseases (Andersson, 2018), cancer (Poprac et al, 2017), neurodegenerative disorders (Jiang et al, 2016), and other nervous system diseases (D'Amico et al, 2013;Patel, 2016;Pei and Fan, 2017). Moreover, oxidative stress also participates in pathological processes after ICH (Aronowski and Zhao, 2011).…”

Section: Discussionmentioning

confidence: 99%

Luteolin Exerts Neuroprotection via Modulation of the p62/Keap1/Nrf2 Pathway in Intracerebral Hemorrhage

Tan

et al. 2020

Front. Pharmacol.

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Upregulation of neuronal oxidative stress is involved in the progression of secondary brain injury (SBI) following intracerebral hemorrhage (ICH). In this study, we investigated the potential effects and underlying mechanisms of luteolin on ICH-induced SBI. Autologous blood and oxyhemoglobin (OxyHb) were used to establish in vivo and in vitro models of ICH, respectively. Luteolin treatment effectively alleviated brain edema and ameliorated neurobehavioral dysfunction and memory loss in vivo. Also, in vivo, we found that luteolin promoted the activation of the sequestosome 1 (p62)/kelch-like enoyl-coenzyme A hydratase (ECH)-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway by enhancing autophagy and increasing the translocation of Nrf2 to the nucleus. Meanwhile, luteolin inhibited the ubiquitination of Nrf2 and increased the expression levels of downstream antioxidant proteins, such as heme oxygenase-1 (HO-1) and reduced nicotinamide adenine dinucleotide phosphate (NADPH): quinine oxidoreductase 1 (NQO1). This effect of luteolin was also confirmed in vitro, which was reversed by the autophagy inhibitor, chloroquine (CQ). Additionally, we found that luteolin inhibited the production of neuronal mitochondrial superoxides (MitoSOX) and alleviated neuronal mitochondrial injury in vitro, as indicated via tetrachloro-tetraethylbenzimidazol carbocyanine-iodide (JC-1) staining and MitoSOX staining. Taken together, our findings demonstrate that luteolin enhances autophagy and anti-oxidative processes in both in vivo and in vitro models of ICH, and that activation of the p62-Keap1-Nrf2 pathway, is involved in such luteolin-induced neuroprotection. Hence, luteolin may represent a promising candidate for the treatment of ICH-induced SBI.

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Section: Discussionmentioning

confidence: 99%

Luteolin Exerts Neuroprotection via Modulation of the p62/Keap1/Nrf2 Pathway in Intracerebral Hemorrhage

Tan

et al. 2020

Front. Pharmacol.

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“…In addition, reactive nitrogen species (RNS), such as peroxynitrite (ONOO − ) and nitric oxide (NO • ), are also thought to be mediators of synovial tissue and joint destruction in RA patients [ 28 , 29 ]. ROS production, lipid peroxidation, protein oxidation and DNA damage were increased in the peripheral blood of RA patients, and antioxidant levels, such as the iron reduction ability and DPPH radical quenching ability, were significantly decreased [ 13 , 30 ].…”

Section: The Production Of Ros In Synovitismentioning

confidence: 99%

The Role of Reactive Oxygen Species in the Rheumatoid Arthritis-Associated Synovial Microenvironment

et al. 2022

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Rheumatoid arthritis (RA) is an inflammatory disease that begins with a loss of tolerance to modified self-antigens and immune system abnormalities, eventually leading to synovitis and bone and cartilage degradation. Reactive oxygen species (ROS) are commonly used as destructive or modifying agents of cellular components or they act as signaling molecules in the immune system. During the development of RA, a hypoxic and inflammatory situation in the synovium maintains ROS generation, which can be sustained by increased DNA damage and malfunctioning mitochondria in a feedback loop. Oxidative stress caused by abundant ROS production has also been shown to be associated with synovitis in RA. The goal of this review is to examine the functions of ROS and related molecular mechanisms in diverse cells in the synovial microenvironment of RA. The strategies relying on regulating ROS to treat RA are also reviewed.

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“…Cartilage degeneration, abnormal synovial hyperplasia progressing to fibroblast‐like synoviocytes in rheumatoid arthritis (RA‐FLSs) that invade the cartilage and bone surface, and subchondral bone erosion are the main pathological features of RA . Studies have shown that oxidative stress is a known critical risk factor in the pathogenesis of RA, is present throughout the occurrence and development of RA, and promotes the progression of the disease . Oxidative stress is a state in which the balance of reactive oxygen species (ROS) produced by endogenous antioxidant systems is disrupted .…”

Section: Introductionmentioning

confidence: 99%

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

Zhang

Wang

et al. 2019

Annals of the New York Academy of Sciences

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Resveratrol (Res) is a polyphenolic compound that has a variety of biological functions and activities. This study aimed to explore the mechanisms of the antioxidant and proapoptotic effects of Res in H2O2‐treated rheumatoid arthritis fibroblast‐like synoviocytes (RA‐FLSs) by the Nrf2–Keap1 signaling pathway. We found that 5 µM H2O2 promoted cell proliferation and increased intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) content in RA‐FLSs. However, Res could reverse these effects in 5 µMH2O2‐treated RA‐FLSs by (1) promoting expression of nuclear factor erythroid 2–related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1), (2) reducing expression of Kelch‐like ECH–related protein 1 (Keap1), (3) inhibiting production of ROS and MDA, (4) blocking activation of nuclear factor‐κB (NF‐κB) p65, (5) inhibiting cell proliferation and migration, and (6) activating Bcl‐2/Bax to induce apoptosis. After lentiviral silencing of Nrf2 (siNrf2) mRNA expression in RA‐FLSs, Res addition did not increase the expression of Nrf2 or HO‐1 to reduce the production of mitochondrial ROS caused by 5 µM H2O2. Res reduced the Bcl‐2/Bax ratio, but siNrf2 reduced the ability of Res to promote apoptosis. We conclude that Res inhibits ROS production by activating the Nrf2 pathway, thereby inhibiting activation of NF‐κB and proliferation and migration of RA‐FLSs, to induce apoptosis. Targeting the Nrf2–Keap1 pathway may be a relevant aim of using Res in the treatment of RA.

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Association of oxidative stress with clinical characteristics in patients with rheumatoid arthritis

Cited by 13 publications

References 46 publications

Luteolin Exerts Neuroprotection via Modulation of the p62/Keap1/Nrf2 Pathway in Intracerebral Hemorrhage

Luteolin Exerts Neuroprotection via Modulation of the p62/Keap1/Nrf2 Pathway in Intracerebral Hemorrhage

The Role of Reactive Oxygen Species in the Rheumatoid Arthritis-Associated Synovial Microenvironment

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

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