Effect of hyaluronic acid (MW 500–730kDa) on proteoglycan and nitric oxide production in human osteoarthritic chondrocyte cultures exposed to hydrostatic pressure

Fioravanti, Antonella; Cantarini, Luca; Chellini, Federico; Manca, D.; Paccagnini, Eugenio; Marcolongo, Roberto; Collodel, Giulia

doi:10.1016/j.joca.2005.03.006

Cited by 35 publications

(19 citation statements)

References 38 publications

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“…Statistical significance was analyzed by the unpaired t test (*p \ 0.05 vs. control group) suppression of PGE 2 production. It has been reported that HA inhibited PGE 2 production in chondrocytes [11], which is consistent with our results.…”

Section: Discussionsupporting

confidence: 94%

High molecular weight hyaluronic acid relieved joint pain and prevented the progression of cartilage degeneration in a rabbit osteoarthritis model after onset of arthritis

Hashizume¹,

Koike²,

Yoshida³

et al. 2010

Mod Rheumatol

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We examined the therapeutic effect of high molecular weight hyaluronic acid (HA) on the progression of joint pain and cartilage degeneration in a rabbit osteoarthritis (OA) model. The OA model was induced by partial meniscectomy. In the time course study, cartilage degeneration was assessed at 3, 7 and 14 days after operation. In the therapeutic study, HA or loxoprofen (LOX) was administered for 14 days beginning four days after operation (after the onset of knee pain and cartilage degeneration). Knee pain was assessed by weight distribution on the hind paw, and cartilage damage and MMP production in the joints were evaluated 18 days after surgery. In the time course study, severe cartilage damage was found three days after operation. In the treatment study, weight-bearing on the injured paw in the control group decreased with time from four days after the operation. However, HA or LOX treatment beginning four days after the operation normalized the reduced hind paw weight distribution, and PGE(2) production was inhibited by HA treatment and LOX treatment. HA significantly inhibited cartilage degeneration, whereas LOX did not. HA also suppressed the production of MMP in joints. Treatment of HA after the onset of cartilage destruction and pain showed a cartilage protective effect as well as an analgesic effect.

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Section: Discussionsupporting

confidence: 94%

High molecular weight hyaluronic acid relieved joint pain and prevented the progression of cartilage degeneration in a rabbit osteoarthritis model after onset of arthritis

Hashizume¹,

Koike²,

Yoshida³

et al. 2010

Mod Rheumatol

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“…Studies of other inflammation‐related cellular systems also support NO production being modulated by HA depending on molecular weight, namely: IL‐1beta‐induced NO production from cartilage cells of osteoarthritic patients being decreased by HMW HA,72 nitrite concentration of synovial fluid of patients increasing as LMW‐HA also concomitantly increases in inflamed joints,73 and NO synthase induction in microglia from neonatal rats induced by 500–800 kDa HA and synergized by interferon‐gamma 74. Another report, however, says that 500–730 kDa HA suppresses IL‐1beta‐induced NO production from human osteoarthritis chondrocytes 75. Thus, there is no agreement in the literature as to the exact conditions or degree to which HA may suppress or enhance the inflammatory production of NO.…”

Section: Discussionmentioning

confidence: 99%

“…74 Another report, however, says that 500-730 kDa HA suppresses IL-1beta-induced NO production from human osteoarthritis chondrocytes. 75 Thus, there is no agreement in the literature as to the exact conditions or degree to which HA may suppress or enhance the inflammatory production of NO. Our data does not support direct enhancement of NO production from RAW 264.7 by LMW-HA, but does demonstrate a mild inhibition under existing strong inflammatory stimulation with LPS and mrIFN-c by HMW-HA.…”

Section: Discussionmentioning

confidence: 99%

Low molecular weight hyaluronic acid effects on murine macrophage nitric oxide production

Lyle

Breger

Baeva

et al. 2010

J Biomedical Materials Res

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Hyaluronic acid (HA) is increasingly used for a number of medical device applications. Since the chemical structure of HA is identical no matter its bacterial or animal origin, it should be the ideal biomaterial. However, short term transient inflammatory reactions are common, while rare long-term adverse events may correlate with subclinical chronic inflammation. Concern has been raised that low molecular weight components or degradation fragments from implanted HA may directly stimulate inflammatory reactions. This study examined a panel of HA molecular weights from the unitary disaccharide up to 1.7 x 10(6) Dalton lengths, in which endotoxin was assayed at a very low level (less than 0.03 EU/mg). The murine cell line RAW 264.7, rat splenocytes, and rat adherent differentiated primary macrophages were assayed for nitric oxide production under a variety of inflammatory conditions plus or minus HA. Under the highest inflammatory states, nitric oxide production was mildly suppressed by HMW-HA while slightly augmented by LMW-HA at mg/mL concentrations. However, at micromolar concentrations fragments below 5000 Daltons, thought to have drug-like qualities, were without effect. These data support the hypothesis that if endotoxin is reduced to an extremely low level, LMW-HA may not directly provoke normal tissue macrophage-mediated inflammatory reactions.

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“…NO inhibits biosynthesis of type II collagen at a post-translational level by activating prolyl hydroxylase and so inducing the hydroxylation of proline residues. The presence of hyaluronic acid (HA) in synovial fluid may counteract this catabolic effect by inhibiting IL-1 -stimulated NO synthesis [14]; however, the disruption of HA in OA may lead to loss of this potentially protective HA effect. The ability of NO to induce chondrocyte apoptosis, as discussed later, further impedes the process of matrix synthesis by reducing the number of resident cells potentially available to participate in cartilage maintenance.…”

Section: Effects Of No On Oa Chondrocytesmentioning

confidence: 99%

Nitric oxide synthases and osteoarthritis

Scher

Pillinger²,

Abramson

2007

Curr Rheumatol Rep

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The production of nitric oxide (NO) by chondrocytes is increased in human osteoarthritis. The excessive production of NO inhibits matrix synthesis and promotes its degradation. Furthermore, by reacting with oxidants such as superoxide anion, NO promotes cellular injury and renders the chondrocyte susceptible to cytokine-induced apoptosis. Thus, NO produced by activated chondrocytes in diseased cartilage may modulate disease progression in osteoarthritis and should therefore be considered a potential target for therapeutic intervention.

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Effect of hyaluronic acid (MW 500–730kDa) on proteoglycan and nitric oxide production in human osteoarthritic chondrocyte cultures exposed to hydrostatic pressure

Abstract: These in vitro studies confirm both the protective role of HA (MW 500-730 kDa), which counteracts the IL-1beta-induced effects, and the importance of pressure on chondrocyte metabolism and morphology.

Cited by 35 publications

References 38 publications

High molecular weight hyaluronic acid relieved joint pain and prevented the progression of cartilage degeneration in a rabbit osteoarthritis model after onset of arthritis

High molecular weight hyaluronic acid relieved joint pain and prevented the progression of cartilage degeneration in a rabbit osteoarthritis model after onset of arthritis

Low molecular weight hyaluronic acid effects on murine macrophage nitric oxide production

Nitric oxide synthases and osteoarthritis

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