Hyaluronic acid inhibits interleukin-1-induced superoxide anion in bovine chondrocytes

Fukuda, Kanji; Takayama, Masaki; Ueno, Mitsuo; Oh, Masamichi; Asada, Shigeki; Kumano, Fumio; Tanaka, Seisuke

doi:10.1007/s000110050132

Cited by 71 publications

(33 citation statements)

References 18 publications

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“…In response to cytokine stimulation, articular chondrocytes have the ability to produce a variety of reactive oxygen species (ROS) including: peroxynitrite, superoxide anion, nitric oxide, and hydrogen peroxide (H202) [7][8][9]191. Furthermore, inflammatory cells and synoviocytes are major sources of ROS.…”

Section: Introductionmentioning

confidence: 99%

Chondrocyte apoptosis induced by hydrogen peroxide requires caspase activation but not mitochondrial pore transition

Kim

2004

Journal Orthopaedic Research

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The primary objective of this study was to test the hypothesis that inhibition of mitochondrial permeability transition andlor inhibition of caspase family enzymes can block chondrocyte apoptosis induced by H202. Primary human chondrocytes were isolated from normal cartilage by enzymatic digestion. Apoptosis was induced by exposure to H202. Chondrocyte apoptosis was quantified using an ELISA for nucleosome formation. Independent confirmation of apoptosis was obtained by TUNEL analysis. H202 induced apoptosis in primary human chondrocytes in a time and dose dependent manner. The effects of candidate apoptosis inhibitors were then tested. Chondrocytes were pretreated with inhibitors of mitochondrial permeability transition, or one of three different caspase inhibitors, and then incubated with H202. Apoptosis was then measured after 16 h of exposure to H202. Pretreatment with inhibitors of mitochondrial permeability transition did not block apoptosis induced by H202. A non-selective caspase inhibitor, a caspase 3-selective inhibitor, and a caspase 1-selective inhibitor, all blocked chondrocyte apoptosis induced by H202. These results show that H 2 0 2 triggers chondrocyte apoptosis through caspase activation, independent of mitochondrial membrane permeability transition.

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Section: Introductionmentioning

confidence: 99%

Chondrocyte apoptosis induced by hydrogen peroxide requires caspase activation but not mitochondrial pore transition

Kim

2004

Journal Orthopaedic Research

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“…Intraarticular bleeding, a source of cytotoxic oxygen metabolites inhibits proteoglycan synthesis and induces chondrocyte death (7). Hyaluronic acid protects cartilage from proinflammatory cytokine-induced ROS by its antioxidant activities (8,9). NO is a mediator of cytokine-induced matrix metalloproteinase (10, 11)-dependent cartilage degradation and a promoter of chondrocyte apoptosis (12).…”

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confidence: 99%

Thiol Antioxidant, N-Acetylcysteine, Activates Extracellular Signal-Regulated Kinase Signaling Pathway in Articular Chondrocytes

Dehnade

Zafarullah

2000

Biochemical and Biophysical Research Communications

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“…HA was shown to promote wound healing (39,40) and attenuating inflammatory processes (18)(19)(20)(41)(42)(43). Also, the interaction of some ligands, including antibodies with the hyaluronate cell surface receptor CD44 on phagocytes, was shown to modulate their inflammatory response (33,44,45).…”

Section: Discussionmentioning

confidence: 99%

Attenuation of the oxidative burst-induced DNA damage in human leukocytes by hyaluronan

Halicka

Mitlitski²,

Heeter³

et al. 2009

Int J Mol Med

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Abstract. Oxidative burst provides the mechanism for specialized phagocytes, such as granulocytes or monocytes, to kill invading microorganisms through generation of superoxide anions. However, the oxidants generated during the burst damage DNA of the phagocytes and neighboring cells. Human blood leukocytes treated with phorbol myristate acetate (PMA) are considered to represent the experimental model of induction of oxidative burst. We recently reported that DNA damage in PMA-treated leukocytes is assessed by cytometric analysis of the induction of histone H2AX phosphorylation and Ataxia Telangiectasia Mutated (ATM) activation. In the present study we observed that hyaluronic acid (HA) of average molecular weight (MW) 5.4x10 6 and 2x10 6 at 0.1% (w/v) concentration significantly attenuated H2AX phosphorylation and ATM activation induced in leukocytes during oxidative burst. HA also reduced the intracellular level of PMA-induced reactive oxidants as measured by the ability of cells to oxidize 2',7'-dihydro-dichlorofluorescein-diacetate. No such effect was seen with HA of 6x10 4 MW. The data are consistent with earlier observations that HA of high MW protects DNA from oxidative damage induced by endo-or exogenous oxidants. The anti-oxidant effect of HA seen during oxidative burst also explains its anti-inflammatory effect when used to treat arthritic joints.

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Hyaluronic acid inhibits interleukin-1-induced superoxide anion in bovine chondrocytes

Abstract: HA can afford protection against cartilage degradation, probably acting as a free-radical scavenger.

Cited by 71 publications

References 18 publications

Chondrocyte apoptosis induced by hydrogen peroxide requires caspase activation but not mitochondrial pore transition

Chondrocyte apoptosis induced by hydrogen peroxide requires caspase activation but not mitochondrial pore transition

Thiol Antioxidant, N-Acetylcysteine, Activates Extracellular Signal-Regulated Kinase Signaling Pathway in Articular Chondrocytes

Attenuation of the oxidative burst-induced DNA damage in human leukocytes by hyaluronan

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