The prophylactic effect of aEugenia aqueaextract against oxidative stress and inflammation associated with the development of arthritis in an adjuvant-induced arthritis rat model

2018 ◽  
Vol 9 (12) ◽  
pp. 6643-6651 ◽  
Author(s):  
Eman A. Abd El-Ghffar ◽  
Omayma A. Eldahshan ◽  
Alaa Barakat ◽  
Thomas Efferth
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Autoimmune Disease ◽  
Rat Model ◽  
Prophylactic Effect ◽  
Human Autoimmune Disease ◽  
Adjuvant Induced Arthritis

Rheumatoid arthritis (RA) is the most common human autoimmune disease.

scholarly journals Effect of Nigella sativa Oil in a Rat Model of Adjuvant-Induced Arthritis

Proceedings ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 16
Author(s):  
Cinzia Nasuti ◽  
Laura Bordoni ◽  
Donatella Fedeli ◽  
Rosita Gabbianelli
Keyword(s):  
Rheumatoid Arthritis ◽  
Rat Model ◽  
Nigella Sativa ◽  
Nigella Sativa Oil ◽  
Adjuvant Induced Arthritis

Rheumatoid arthritis is characterized [...]

scholarly journals Anti-arthritic Effects of Oplopanax elatus in a Rat Model of Rheumatoid Arthritis (Adjuvant-induced Arthritis)

2019 ◽  
Vol 25 (4) ◽  
pp. 304
Author(s):  
Ki Sun Kwon ◽  
Hyun Lim ◽  
Yong Soo Kwon ◽  
Hye Ri Choi ◽  
Myong Jo Kim ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Rat Model ◽  
Adjuvant Induced Arthritis ◽  
Oplopanax Elatus

Oleuropein down-regulated IL-1β-induced inflammation and oxidative stress in human synovial fibroblast cell line SW982

2017 ◽  
Vol 8 (5) ◽  
pp. 1890-1898 ◽  
Author(s):  
Maria Luisa Castejón ◽  
Maria Ángeles Rosillo ◽  
Tatiana Montoya ◽  
Alejandro González-Benjumea ◽  
Jose Maria Fernández-Bolaños ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Autoimmune Disease ◽  
Cell Line ◽  
Synovial Fibroblast ◽  
Fibroblast Cell ◽  
Synovial Fibroblasts ◽  
Fibroblast Cell Line ◽  
Inflammatory Autoimmune Disease ◽  
And Oxidative Stress

Rheumatoid arthritis (RA) is a chronic and systemic inflammatory autoimmune disease mainly characterized by aggressive hyperproliferation of synovial fibroblasts (SFs).

scholarly journals Inflammatory and Oxidative Stress Markers—Mirror Tools in Rheumatoid Arthritis

Biomedicines ◽  
2020 ◽  
Vol 8 (5) ◽  
pp. 125 ◽  
Author(s):  
Radu Răzvan Mititelu ◽  
Rodica Pădureanu ◽  
Manuela Băcănoiu ◽  
Vlad Pădureanu ◽  
Anca Oana Docea ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Autoimmune Disease ◽  
Joint Destruction ◽  
Protein Carbonyl ◽  
Thiobarbituric Acid Reactive Substance ◽  
Oxidative Stress Biomarkers ◽  
Neutrophil Lymphocyte Ratio ◽  
Lymphocyte Ratio ◽  
Inflammatory Status

Rheumatoid arthritis (RA) is a chronic progressive autoimmune disease, associated with significant morbidity, mainly due to progressive damage and consequent disability. Oxidative stress is an important part of RA pathophysiology, as in autoimmune disease the interaction between immune response and endogenous/exogenous antigens subsequently induce the production of reactive oxygen species. The oxidative stress process seems to be positively strongly correlated with inflammation and accelerated joint destruction. We were asking ourselves if the oxidative stress biomarkers are the mirror tools of disease activity, outcome, and inflammation level in a group of RA patients under standard or biological therapy compared to healthy age-matched controls. In order to do this, the oxidative stress damage biomarkers (lipids peroxide and protein carbonyl level), antioxidant defense capacity, and pro-inflammatory status of plasma were quantified. In this study, we took into account the complete picture of RA diseases and assessed, for the first time, the inflammatory level in correlation with the oxidative stress level and antioxidant capacity of RA patients. Our results revealed that protein oxidation through carbonylation is significantly increased in RA groups compared to controls, and both protein carbonyl Pcarb and thiobarbituric acid reactive substance (TBARS) are reliable markers of ROS damage. Therefore, it is unanimous that neutrophil/lymphocyte ratio (NLR), monocyte/lymphocyte ratio (MLR), platelet/lymphocyte ratio (PltLR) correlated with Pcarb, and TBARS can provide a view of the complex phenomenon represented by proteins/lipids damage, key contributors to disease outcome, and an increased awareness should be attributed to these biomarkers.

scholarly journals Eccentric training enhances the αB-crystallin binding to the myofibrils and prevents skeletal muscle weakness in adjuvant-induced arthritis rat

2019 ◽  
Vol 127 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Koichi Himori ◽  
Daisuke Tatebayashi ◽  
Yuki Ashida ◽  
Takashi Yamada
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Strength ◽  
Muscle Weakness ◽  
Eccentric Contractions ◽  
Eccentric Training ◽  
Adjuvant Induced Arthritis ◽  
Skeletal Muscle Weakness ◽  
Αb Crystallin

Patients with rheumatoid arthritis (RA) frequently suffer from muscle weakness. We examined whether eccentric training prevents skeletal muscle weakness in adjuvant-induced arthritis (AIA) rat, a widely used animal model for RA. AIA was induced in the knees of Wistar rats by injection of complete Freund’s adjuvant. To induce eccentric contractions (ECCs), neuromuscular electrical stimulation (45 V) was applied to the plantar flexor muscles simultaneously with forced dorsiflexion of the ankle joint (0–40°) and was given every 6 s. ECC exercise was applied every other day for a total of 11 sessions and consisted of 4 sets of 5 contractions. There was a significant reduction in in vitro maximum Ca2+-activated force in skinned fibers in gastrocnemius muscle from AIA rats. These changes were associated with reduced expression levels of contractile proteins (i.e., myosin and actin), increased levels of inflammation redox stress-related biomarkers (i.e., TNF-α, malondialdehyde-protein adducts, NADPH oxidase 2, and neuronal nitric oxide synthase), and autolyzed active calpain-1 in AIA muscles. ECC training markedly enhanced the steady-state levels of αB-crystallin, a small heat shock protein, and its binding to the myofibrils and prevented the AIA-induced myofibrillar dysfunction, reduction in contractile proteins, and inflammation-oxidative stress insults. Our findings demonstrate that ECC training preserves myofibrillar function without muscle damage in AIA rats, which is at least partially attributable to the protective effect of αB-crystallin on the myofibrils against oxidative stress-mediated protein degeneration. Thus ECC training can be a safe and effective intervention, counteracting the loss of muscle strength in RA patients. NEW & NOTEWORTHY Eccentric contractions (ECCs) are regarded as an effective way to increase muscle strength. No studies, however, assess safety and effectiveness of ECC training on muscle weakness associated with rheumatoid arthritis. Here, we used adjuvant-induced arthritis (AIA) rats to demonstrate that ECC training prevents intrinsic contractile dysfunction without muscle damage in AIA rats, which may be attributed to the protective effect of αB-crystallin on the myofibrils against inflammation-oxidative stress insults.

scholarly journals NEUROGENIC MODULATION BY NEUROKININ-1 RECEPTOR ANTAGONIST, CP-96,345 TO INHIBIT RHEUMATOID ARTHRITIS DEVELOPMENT IN ADJUVANT INDUCED ARTHRITIS RAT MODEL

2017 ◽  
Vol 52 (2) ◽  
pp. 87
Author(s):  
Yuyun Wirasasmita ◽  
Mahardian Rahmadi ◽  
Imam Susilo ◽  
Junaidi Khotib
Keyword(s):  
Rheumatoid Arthritis ◽  
Substance P ◽  
Response Time ◽  
Rat Model ◽  
Neurogenic Inflammation ◽  
Receptor Expression ◽  
Joint Tissue ◽  
Neurokinin 1 Receptor ◽  
Adjuvant Induced Arthritis ◽  
Neurokinin 1

Rheumatoid arthritis (RA) is a chronic form of persistent inflammation. Meanwhile, Substance P is the most associated neuropeptide in neurogenic inflammation and hyperalgesia commonly found in chronic pain. Substance P act by binding to neurokinin-1 receptor. The present study was conducted to evaluate the effect of neurokinin-1 receptor antagonist (CP-96,345) on Adjuvant Induced Arthritis rat model, induced by Complete Freund’s Adjuvant (CFA). The objective is to attenuate neurogenic inflammation which in turn will increase the latency time of hyperalgesia response, decreases neurokinin-1 receptor expression, and inhibits the development of RA in AIA rat model. Rats were intra-articularly injected with CFA 1 hour after the administration of CP-96,345 either by 0.63 µg/gr; 1.25 µg/gr; or 2.5 µg/gr also intra-articularly. Caliper measurements and hot-plate test were performed on day 0, 3, 5, 7, 9, 11, and day 13. Expression of neurokinin-1 receptor in joint tissue were evaluated by immunohistochemistry, and RA progress in joint tissue were observed hystopathologically. CP-96,345 at 2.5 µg/gr significantly increases the latency of hyperalgesia response time on CFA induced rats (p=0.044) and decreased the neurokinin-1 receptor expression in joint tissue (p=0.029) compared to CFA induced rats. There was no significant difference for caliper measurements and RA progress between CFA incduced rats and treated group. Conclusively, CP-96,345 increases the latency of hyperalgesia response time and decreases the NK-1 receptor expression in rat joint but could not inhibit RA progression.

Protective Effect of Swertiamarin on Myocardial Injury Through Activation of Nrf2/HO-1 Pathway in Heart Failure Model of Rats

2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Protective Effect ◽  
Infarct Size ◽  
Rat Model ◽  
Left Ventricular ◽  
Related Factor ◽  
Nuclear Factor ◽  
Internal Dimension

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.

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