Chinese Journal of Tissue Engineering Research ›› 2013, Vol. 17 ›› Issue (2): 247-253.doi: 10.3969/j.issn.2095-4344.2013.02.011

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Monosodium iodoacetate induces apoptosis of primary rat chondrocytes

Jiang Li-ping1, Li Long-jie2, Gong De-zheng1, Geng Cheng-yan1, Jiang Li-jie3, Zhong Lai-fu1   

  1. 1  China-Japanese Joint Institute for Medical and Pharmaceutical Science, Dalian Medical University, Dalian  116044, Liaoning Province, China
    2  Department of Radiotherapy Oncology, First Affiliated Hospital of Dalian Medical University, Dalian  116023, Liaoning Province, China
    3  Department of Medicine, Affiliated Zhongshan Hospital of Dalian University, Dalian  116001, Liaoning Province, China
  • Received:2012-04-02 Revised:2012-05-12 Online:2013-01-08 Published:2013-01-08
  • Contact: Zhong Lai-fu, Professor, Doctoral supervisor, China-Japanese Joint Institute for Medical and Pharmaceutical Science, Dalian Medical University, Dalian 116044, Liaoning Province, China
  • About author:Jiang Li-ping★, Master, Senior experimentalist, China-Japanese Joint Institute for Medical and Pharmaceutical Science, Dalian Medical University, Dalian 116044, Liaoning Province, China dljlp@yahoo.cn

Abstract:

BACKGROUND: Recently, monosodium iodoacetate is usually used to cause cartilage degradation resembling the pathological changes of human osteoarthritis. However, rate studies report the mechanisms underlying monosodium iodoacetate-induced chondrocyte apoptosis.  
OBJECTIVE: To assess the apoptosis of primary rat chondrocytes induced by different concentrations of monosodium iodoacetate and to clarify the underlying mechanism.
METHODS: The primary rat chondrocytes were treated with monosodium iodoacetate for 24 hours, and the induction of apoptosis was analyzed by flow cytometry and Hoechst 33342/PI staining. The levels of mitochondrial membrane potential were evaluated using fluorescence spectrophotometer and laser scanning confocal microscope. The production of reactive oxygen species was determined by fluorescence spectrophotometer. Apoptosis-related protein cytochrome C and caspase-3 expressions were examined by western blotting.
RESULTS AND CONCLUSION: Monosodium iodoacetate induced cellular apoptosis in a dose-dependent manner. Significantly increased level of reactive oxygen species was observed in primary rat chondrocytes at higher concentration of monosodium iodoacetate (P < 0.05). Significantly decreased levels of mitochondrial membrane potential were also shown in primary rat chondrocytes (P < 0.05). Western blot assay revealed that monosodium iodoacetate significantly increased the release of cytochrome C and the protein expression of caspase-3, leading to cell apoptosis. Together these observations suggest that the mechanisms of monosodium iodoacetate-induced apoptosis are primarily via the production of reactive oxygen species and mitochondria- mediated caspase-3 activation in primary rat chondrocytes.

Key words: tissue construction, cartilage tissue construction, chondrocytes, monosodium iodoacetate, reactive oxygen species, mitochondrial membrane potential, cytochrome C, Caspase-3, apoptosis

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