High molecular weight hyaluronic acid inhibits advanced glycation endproduct‐induced NF‐κB activation and cytokine expression

Neumann, Arne; Schinzel, Reinhard; Palm, D.; Riederer, Peter; Münch, Gerald

doi:10.1016/s0014-5793(99)00731-0

Cited by 185 publications

(127 citation statements)

References 41 publications

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“…It has also been linked to states of anti-oxidant depletion induced by AGE, with a reduction in glutathione, vitamin C and nitric oxide [66]. Further evidence of an interaction between AGE and the NF-kB pathway can be shown from in vitro studies using hyaluronic acid, which is a glycosaminoglycan polymer that inhibits AGE-induced activation of NF-kB and NF-kB regulated release of IL-1a, IL-6 and TNFa [67].…”

Section: R2mentioning

confidence: 99%

Advanced glycation end-products: a review

et al. 2001

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Diabetes is a common condition with multiple complications. There has been much work done to elaborate on the aetiology, prevention and treatment of diabetes related complications. The DCCT [1] and UKPDS [2] studies have emphasised the role of tight glucose control as being important in reducing diabetic microvascular disease in Type I (insulin-dependent) diabetes mellitus (DCCT) and Type II (non-insulin-dependent) diabetes mellitus (UKPDS). The relation between tight glucose control and macrovascular complications is, however, not clear [3]. Recently the importance of blood pressure control in reducing diabetic microvascular complications has been shown [4]. Apart from these factors, damage induced by hyperglycaemia involves a complex interaction between many influences including genetic predisposition, smoking, BMI, dyslipidaemia and alterations in coagulation factors [3]. The presence of advanced glycation end-products (AGE) is closely related to Diabetologia (2001) AbstractAdvanced glycation end-products are a complex and heterogeneous group of compounds that have been implicated in diabetes related complications. At present it is not known if they are the cause or the consequence of the complications observed. We discuss the chemistry of advanced glycated end-product formation and their patho-biochemistry particularly in relation to the diabetic microvascular complications of retinopathy, neuropathy and nephropathy as well as their role in the accelerated vasculopathy observed in diabetes. The concept of carbonyl stress as a cause for advanced glycated end-product toxicity is mentioned. We discuss alterations in the concentrations of advanced glycated end-products in the body, particularly in relation to changes occuring with age, diabetes and its complications such as nephropathy. Problems relating to current methods of advanced glycated end-product detection and measurement are highlighted including the lack of a universally established method of detection or unit of measurement. Agents used for the treatment of advanced glycated end-product accumulation are reviewed, with an emphasis on the results of the recent phase III trials using aminoguanidine and diabetes related complications. [Diabetologia (2001) 44: 129±146]Keywords Advanced glycated end-products, diabetes mellitus, microvascular disease, carbonyl stress, aminoguanidine.Corresponding author: Dr R. Singh MRCP (UK), FRACP, University Dept of Medicine, Royal Perth Hospital, PO Box X2213, Perth 6847, Western Australia Abbreviations: ESRD, End-stage renal disease; 3-DG, 3-deoxyglucosone; MGO, methylglyoxal; DOLD, deoxyglucosone-lysine dimer; MOLD, methyl glyoxal-lysine dimer; CML, N e -[carboxymethyl]-lysine; FFI, furoyl-furanyl imidazole; PTB, phenacyl thiozolium bromide; RAGE, receptor for AGE; NF-kB, nuclear factor-kB; VCAM-1, vascular cell adhesion molecule-1; ICAM-1, intracellular adhesion molecule-1; PECAM-1, platelet endothelial cell adhesion molecule-1; ELAM-1, endothelial leucocyte adhesion molecule-1; MSR, macrophage scavenger recepto...

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Section: R2mentioning

confidence: 99%

Advanced glycation end-products: a review

et al. 2001

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“…From these findings, interaction between HA and CD44 probably caused significant suppression of LPS-induced PGE 2 production and p65 NF-κ B phosphorylation. Functional HA-CD44 interaction that causes NF-κ B down-regulation in activated macrophages is supported by additional data that anti-CD44 antibody cancels the inhibitory effect of HA on AGE-induced translocation of NF-κ B complex into the nucleus in J774 mouse macrophages (Neumann et al 1999). In RA synovial tissues, CD44 (Aruffo et al 1990) and ICAM-1 (Klimiuk et al 2002) are over-expressed in proportion to the severity of synovial inflammation, suggesting the critical roles of HA receptors in the pathology of RA.…”

Section: Discussionmentioning

confidence: 82%

“…Therefore, PGE 2 is considered to be produced in association with COX-2 up-regulation in RA synovium through NF-κ B activation. In J774 mouse macrophages, HA can inhibit advanced glycation end product (AGE)-induced expression of proinflammatory cytokines and NF-κ B nuclear translocation (Neumann et al 1999). This study extended our previous findings (Yasuda 2007) and has shown that HA inhibits PGE 2 production by COX-2 suppression through down-regulation of NF-κ B in LPS-activated U937 cells.…”

Section: Discussionmentioning

confidence: 99%

Hyaluronan Inhibits Prostaglandin E2 Production via CD44 in U937 Human Macrophages

Yasuda

2010

Tohoku J. Exp. Med.

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“…Microglia and astroglia try in vain to degrade senile plaques, thereby generating free radicals as well as proinflammatory cytokines like interleukin 1 and 6, but also tumor-necrosis factor alpha (TNF-a). Thereby adjacent nervous tissue is damaged (Neumann et al, 1999). In addition to these inflammatory processes other factors, like an age-and stress-dependent energy deficit, contribute to the diminished ability of the neurons to cope with free radicals as well as to repair damaged structures (Blum-Degen et al, 1995;Hoyer, 1991).…”

Section: Discussionmentioning

confidence: 99%

Alpha-lipoic acid as a new treatment option for Azheimer type dementia

Häger¹,

Marahrens²,

Kenklies³

et al. 2001

Archives of Gerontology and Geriatrics

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167

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Oxidative stress and energy depletion are characteristic biochemical hallmarks of Alzheimer's disease (AD), thus antioxidants with positive effects on glucose metabolism such as thioctic (a-lipoic) acid should exert positive effects in these patients. Therefore, 600 mg a-lipoic acid was given daily to nine patients with AD and related dementias (receiving a standard treatment with acetylcholinesterase inhibitors) in an open study over an observation period of, on avarage, 337 980 days. The treatment led to a stabilization of cognitive functions in the study group, demonstrated by constant scores in two neuropsychological tests (mini-mental state examination: MMSE and AD assessment scale, cognitive subscale: ADAScog). Despite the fact that this study was small and not randomized, this is the first indication that treatment with a-lipoic acid might be a successful 'neuroprotective' therapy option for AD and related dementias.

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High molecular weight hyaluronic acid inhibits advanced glycation endproduct‐induced NF‐κB activation and cytokine expression

Cited by 185 publications

References 41 publications

Advanced glycation end-products: a review

Advanced glycation end-products: a review

Hyaluronan Inhibits Prostaglandin E2 Production via CD44 in U937 Human Macrophages

Alpha-lipoic acid as a new treatment option for Azheimer type dementia

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