Chondrocyte apoptosis following intraarticular fracture in humans

Aims: The protective effects of ginger (Zingiber officinale Roscoe) extract on IL-1β-mediated oxidative stress and mitochondrial apoptosis were investigated in C28I2 human chondrocytes. Methods: The effects of various concentrations of ginger extract on C28I2 human chondrocyte viability were evaluated in order to obtain noncytotoxic concentrations of the drug by methylthiotetrazole assay. The cells were pretreated with 5 and 25 μg/mL ginger extract for 24 h, followed by incubation with IL-1β (10 ng/mL) for 24 h. The effects of ginger extract on IL-1β-induced intracellular reactive oxygen species (ROS) production and lipid peroxidation were examined. The mRNA expressions of antioxidant enzymes including catalase, superoxide dismutase-1, glutathione peroxidase-1, glutathione peroxidase-3, and glutathione peroxidase-4 were evaluated by reverse transcription polymerase chain reaction. The protein expressions of Bax, Bcl-2, and caspase-3 were analyzed by Western blotting. Results: No cytotoxicity was observed at any concentration of ginger extract in C28I2 cells. Ginger extract pretreatment remarkably increased the gene expression of antioxidant enzymes and reduced the IL-1β-induced elevation of ROS, lipid peroxidation, the Bax/Bcl-2 ratio, and caspase-3 activity. Conclusions: Ginger extract could considerably reduce IL-1β-induced oxidative stress and consequent mitochondrial apoptosis as the major mechanisms of chondrocyte cell death. These beneficial effects of ginger extract may be due to its antioxidant properties. It may be considered as a natural herbal product to prevent OA-induced cartilage destruction in the clinical setting.

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“…Many studies have indicated significant correlations between OA grade and chondrocyte apoptosis [Kim et al, 2002].…”

Section: Ginger ( Z Officinalementioning

confidence: 99%

Protective Effect of Ginger (Zingiber officinale Roscoe) Extract against Oxidative Stress and Mitochondrial Apoptosis Induced by Interleukin-1β in Cultured Chondrocytes

Hosseinzadeh

Juybari

Fatemi

et al. 2017

Cells Tissues Organs

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“…It is well established that wounding of articular cartilage leads to apoptotic and necrotic cell death at the lesion edge [2][3][4][5][6][7] ; thus, cartilage tissue integration is likely impaired by a lack of live or viable cells at the interface region that are capable of producing a functional repair tissue. 8,9 In addition, this is hindered by the inherent limited ability of chondrocytes to migrate through the extracellular matrix toward the acellular interface region.…”

Section: Introductionmentioning

confidence: 99%

Enhanced Tissue Integration During Cartilage Repair In Vitro Can Be Achieved by Inhibiting Chondrocyte Death at the Wound Edge

Gilbert

Singhrao

Khan

et al. 2009

Tissue Engineering Part A

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“…Chondrocyte apoptosis has also been shown in human biopsy tissue near sites of chondral fracture [15]. Canine cartilage explants subjected to 5 MPa of cyclic compression at 0.3 Hz exhibited the development of both necrosis and apoptosis, increasing progressively with load duration and time.…”

Section: Resultsmentioning

confidence: 91%

The limitation of acute necrosis in retro-patellar cartilage after a severe blunt impact to the in vivo rabbit patello-femoral joint

et al. 2005

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We have previously shown that surface lesions and acute necrosis of chondrocytes are produced by severe levels of blunt mechanical load, generating contact pressures greater than 25 MPa, on chondral and osteochondral explants. We have also found surface lesions and chronic degradation of retro-patellar cartilage within 3 years following a 6 J impact intensity with an associated average pressure of 25 MPa in the rabbit patello-femoral joint. We now hypothesized that cellular necrosis is produced acutely in the retropatellar cartilage in this model as a result of a 6 J impact and that an early injection of the non-ionic surfactant, poloxamer 188 (P188), would significantly reduce the percentage of necrotic cells in the traumatized cartilage. Eighteen rabbits were equally divided into a 'time zero' group and two other groups carried out for 4 days. One '4 day' group was administered a 1.5 ml injection ofel88 into the impacted joint immediately after trauma, while the other was injected with a placebo solution. Impact trauma produced surface lesions on retro-patellar cartilage in all groups. Approximately 15% of retro-patellar chondrocytes suffered acute necrosis in the 'time zero' and '4-day no poloxamer' groups. In contrast, significantly fewer cells (7%) suffered necrosis in the poloxamer group, most markedly in the superficial cartilage layer. The use of P188 surfactant early after severe trauma to articular cartilage may allow sufficient time for damaged cells to heal, which may in turn mitigate the potential for post-traumatic osteoarthritis. Additional studies are needed to improve the efficacy of this surfactant and to determine the long-term health ofjoint cartilage after P188 intervention.

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Chondrocyte apoptosis following intraarticular fracture in humans

Cited by 83 publications

References 11 publications

Protective Effect of Ginger (<b><i>Zingiber officinale</i></b> Roscoe) Extract against Oxidative Stress and Mitochondrial Apoptosis Induced by Interleukin-1β in Cultured Chondrocytes

Protective Effect of Ginger (<b><i>Zingiber officinale</i></b> Roscoe) Extract against Oxidative Stress and Mitochondrial Apoptosis Induced by Interleukin-1β in Cultured Chondrocytes

Enhanced Tissue Integration During Cartilage Repair In Vitro Can Be Achieved by Inhibiting Chondrocyte Death at the Wound Edge

The limitation of acute necrosis in retro-patellar cartilage after a severe blunt impact to the in vivo rabbit patello-femoral joint

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