The effect of hyaluronic acid on IL‐1β‐induced chondrocyte apoptosis in a rat model of osteoarthritis

Abstract

The purpose of this article was to study the effect of hyaluronic acid (HA) on chondrocyte apoptosis in a rat osteoarthritis in vitro model (exposure to IL-1b) and explore its mechanism. A rat in vitro model of osteoarthritis (OA) was established using 10 ng/mL IL-1b as a modulating and chondrocyte apoptosis inducing agent. Different doses of HA (10, 20, and 40 mg/mL) were added 1 h prior to the addition of IL-1b to a monolayer culture of freshly isolated juvenile rat chondrocytes. The ratio of apoptotic cell death was surveyed by Annexin V-FITC and propidium iodide double-labeling FACS analysis. The mitochondrial membrane potential of chondrocytes was evaluated by rhodamine-123 fluorescence. The mitochondrial function was evaluated through detecting the ATP production by a luciferase assay. The reverse transcription polymerase chain reaction (RT-PCR) was performed to measure mRNA expression levels of inducible oxide synthase (iNOS). HA could inhibit IL-1b-induced chondrocyte apoptosis in our cell culture model system. It was showed that addition of HA to the medium was able in a dose-dependent way to reduce the impairment of the mitochondrial membrane potential and to restore mitochondrial ATP production. This study shows that HA could suppress in a dose-dependent way chondrocyte apoptosis in our IL-1b-induced osteoarthritis model. The suppression of inflammatory cytokine activity within the joint might be one important mechanism of the clinical action of intraarticular injection of HA in the treatment of OA. ß

17β-Estradiol promotes cell proliferation in rat osteoarthritis model chondrocytes via PI3K/Akt pathway

“…Thin slices of cartilage were sequentially digested and the resulting cell suspension was transferred to 60 mm culture dishes with Dulbecco's Modified Eagle Medium (DMEM)/F12 containing 10% FBS supplemented with antibiotics: penicillin (100 UI/ml, Sigma) and erythromycin (100 µg/ml, Sigma). Since interleukin-1β (IL-1β) is one of the key proinflammatory cytokines contributing to the progression of OA by stimulating the secretion of several proinflammatory mediators such as prostaglandin E2 (PGE2) and NO that are implicated in the pathogenesis of OA, chondrocytes treated with IL-1β were regarded as an experimental OA cell model [9]. The cells reached subconfluence, the medium was changed to DMEM/F12 with 0.5% FBS and antibiotics, added with recombinant IL-1β (10 ng/ml, Sigma) for 2 hr to imitate OA chondrocytes [9].…”

“…Since interleukin-1β (IL-1β) is one of the key proinflammatory cytokines contributing to the progression of OA by stimulating the secretion of several proinflammatory mediators such as prostaglandin E2 (PGE2) and NO that are implicated in the pathogenesis of OA, chondrocytes treated with IL-1β were regarded as an experimental OA cell model [9]. The cells reached subconfluence, the medium was changed to DMEM/F12 with 0.5% FBS and antibiotics, added with recombinant IL-1β (10 ng/ml, Sigma) for 2 hr to imitate OA chondrocytes [9]. Then, cells were treated with the indicated concentrations The BrdU (5-bromo-2'-deoxyuridine assay) assay Cells were seeded in the 96-well tissue culture plate as required and treated with IL-1β for 2 hr, and then incubated with BrdU for 2 hr according to the manufacturer's instructions (CHEMICON International, Inc.), followed by treatment with or without E2 or Ly294002 for different times.…”

Melanocortin peptides protect chondrocytes from mechanically induced cartilage injury

“…Additionally, OA is featured by reduced cellularity [21,[23][24][25][26][27][28][29], a fact that is thought to contribute to the inability of the remaining chondrocytes to maintain normal matrix synthesis, thereby contributing to cartilage degradation [30].…”

Cationised gelatin and hyaluronic acid coating enhances polyethylene terephthalate artificial ligament graft osseointegration in porcine bone tunnels

“…As a component of the extracellular matrix, hyaluronic acid has been demonstrated to accelerate the healing of rabbit flexor tendons [9]. Particularly, hyaluronic acid has the high capacity to suppress and alleviate inflammation [10][11][12]. Cationised gelatin, as a positively charged polymer, has long been used as a highly valuable carrier system as it provides a universally effective way to enhance biocompatibility of the polymers [13][14][15].…”