Suppression of Type II Collagen-Induced Arthritis by N-Acetyl-l-Cysteine in Mice

Kröger, Hans; Miesel, Ralf; Dietrich, Annette; Ohde, Manuela; Altrichter, Sabine; Braun, Claudia; Ockenfels, H.

doi:10.1016/s0306-3623(96)00570-8

Cited by 27 publications

(23 citation statements)

References 22 publications

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“…Abbreviations are PDGF, platelet-derived growth factor; TNF-a, tumor necrosis factor a, Ox-LDL, oxidized lowdensity lipoprotein; NF-kB, nuclear factor kappa B; NIC, NF-kB-induced kinase; IKK, IkB kinase; IkB, inhibitor of NF-kB; MEK, MAPK/ERK kinase; ERK, extracellular signal-regulated kinase; ELK-1, ets domain protein; MEF2, myocyte enhancer factor 2; ATF2, activating transcription factor 2; TRE, tumor promoter responsive element; AP-1, activator protein-1; SAPK, stress-activated protein kinase; JNK, c-Jun N-terminal kinase. agreement with these in vitro studies, NAC was shown to inhibit collagen-induced arthritis in mice by inhibiting inflammatory cytokines and NF-kB activity [112,113]. In a human exercise model of acute muscle injury, NAC (10 mg/Kg body weight for 7 day post-injury) transiently increased oxidative stress and tissue damage, although effects of chronic use of this supplement are not known [114].…”

Section: N-acetylcysteine In Musculoskeletal System and Arthritismentioning

confidence: 76%

Molecular mechanisms of N -acetylcysteine actions

Zafarullah¹,

Li²,

Sylvester³

et al. 2003

Cellular and Molecular Life Sciences (CMLS)

1,209

879

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Oxidative stress generated by an imbalance between reactive oxygen species (ROS) and antioxidants contributes to the pathogenesis of arthritis, cancer, cardiovascular, liver and respiratory diseases. Proinflammatory cytokines and growth factors stimulate ROS production as signaling mediators. Antioxidants such as N-acetylcysteine (NAC) have been used as tools for investigating the role of ROS in numerous biological and pathological processes. NAC inhibits activation of c-Jun N-terminal kinase, p38 MAP kinase and redox-sensitive activating protein-1 and nuclear factor kappa B transcription factor activities regulating expression of numerous genes. NAC can also prevent apoptosis and promote cell survival by activating extracellular signal-regulated kinase pathway, a concept useful for treating certain degenerative diseases. NAC directly modifies the activity of several proteins by its reducing activity. Despite its nonspecificity, ability to modify DNA and multiple molecular modes of action, NAC has therapeutic value for reducing endothelial dysfunction, inflammation, fibrosis, invasion, cartilage erosion, acetaminophen detoxification and transplant prolongation.

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Section: N-acetylcysteine In Musculoskeletal System and Arthritismentioning

confidence: 76%

Molecular mechanisms of N -acetylcysteine actions

Zafarullah¹,

Li²,

Sylvester³

et al. 2003

Cellular and Molecular Life Sciences (CMLS)

1,209

879

View full text Add to dashboard Cite

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“…It has been suggested that oxidative stress plays an important role in the pathobiology of RA, and the beneficial therapeutic effects of antioxidants have been demonstrated in experimental models of RA [12][13][14][15][16][17]. However, a recent systematic review of randomized clinical trials failed to show a clear effect of antioxidants such as vitamins A, C, and E and selenium, on RA [36].…”

Section: Discussionmentioning

confidence: 99%

“…Lipid peroxidation markers such as serum malondialdehyde and urine isoprostane are reported to be elevated in collagen-induced arthritis (CIA) compared with those in controls [10,11]. The beneficial effects of antioxidants, including vitamin E, tempol, ␣-lipoic acid, N-acetylcysteine, the polyphenolic fraction of green tea, and (−)-epigallocatechin-3-gallate, have been demonstrated in mice with CIA [12][13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Grape seed proanthocyanidin extract (GSPE) attenuates collagen-induced arthritis

et al. 2009

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“…The induction of arthritis significantly increased malondialdehyde (MDA), oxidized proteins such as protein carbonyl (PCO), advanced glycation endproducts (AGE), anti-collagen antibody, rheumatoid factor, interleukin (IL)-1beta, IL-6, and low density lipoprotein in the serum of patients [101]. The antiarthritic and anti-inflammatory efficacy of N-acetyl-L-cysteine (NAC) was tested in male DBA/1 hybrid mice suffering from type II collagen-induced arthritis [102]. After treatment with 100 mg/kg of NAC from day 42 after immunization over a period of six weeks, the ROS production was reduced to levels occurring in whole blood of healthy animals.…”

Section: Role Of Reactive Oxygen Species In Bone Fracturesmentioning

confidence: 99%

Calcium Metabolism and Oxidative Stress in Bone Fractures: Role of Antioxidants

Sheweita

Khoshhal²

2007

CDM

198

152

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Calcium ion is an essential structural component of the skeleton. There is growing evidence for the importance of nutrition in the maintenance of bones and joints health. Nutritional imbalance combined with endocrine abnormalities may be involved in osteoporosis. For example, essential fatty acids and their metabolites were reported to have beneficial action in osteoporosis. The mechanism by which fatty acids prevent osteoporosis may involve inhibition of pro-inflammatory cytokines, which are known to have a major role in osteoporosis through induction of oxidative stress which had adverse effects on the skeleton. Other risk factors for osteoporosis, such as smoking, hypertension and diabetes mellitus are also associated with increased oxidative stress and free radicals levels. When bone fracture occurs, a remarkable yield of free radicals is generated by the damaged tissues. However, controlled production of free radicals by normally functioning osteoclasts could accelerate destruction of calcified tissues and assist bone remodeling. Enhanced osteoclastic activity observed in bone disorders may have been responsible for increased production of reactive oxygen species [ROS] in the form of superoxide, which is evident by increased levels of serum malondialdehyde [MDA] levels. One of the most damaging effects of ROS is lipid peroxidation, the end product of which is MDA which also served as a measure of osteoclastic activity. Inhibition of the antioxidant enzymes activities, such as superoxide dismutase and glutathione peroxidase, was found to increase superoxide production by the osteoclasts which represented by increased levels of MDA. Therefore, oxidative stress is an important mediator of bone loss since deficiency of antioxidant vitamins has been found to be more common in the elderly osteoporotic patients. It is concluded from this review that increased free radical production overwhelms the natural antioxidants defense mechanisms, subjecting individuals to hyperoxidant stress and thus leading to osteoporosis. In addition, administration of antioxidants might protect bones from osteoporosis and also might help in the acceleration of healing of fractured bones.

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Suppression of Type II Collagen-Induced Arthritis by N-Acetyl-l-Cysteine in Mice

Cited by 27 publications

References 22 publications

Molecular mechanisms of N -acetylcysteine actions

Molecular mechanisms of N -acetylcysteine actions

Grape seed proanthocyanidin extract (GSPE) attenuates collagen-induced arthritis

Calcium Metabolism and Oxidative Stress in Bone Fractures: Role of Antioxidants

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