Cytoskeleton remodeling and oxidative stress description in morphologic changes of chondrocyte in Kashin-Beck disease.

Kashin-Beck disease (KBD) is a kind of deformity disease involved in cytoskeleton and inner homeostasis regulation. The enrichment analysis of bioprocess, networks, and related disease set were performed. The development regulation, metabolic process, and apoptosis were important procession in KBD; it revealed the up-regulated process in removal of superoxide radicals, glycolysis and glucose catabolic process, regulation of cytoskeleton rearrangement and phagosome in antigen presentation. Morphological changes of KBD chondrocyte were investigated by transmission electronic microscopy compare with the normal one. The ultrastructure of KBD chondrocyte referred to oxidative stress and metabolic dysfunction has been found.

Proteomic changes in articular cartilage of human endemic osteoarthritis in China.

Kashin-Beck disease (KBD) is a chronic endemic osteochondropathy with unclear pathogenesis. It is a degenerative disease similar to osteoarthritis, but with different manifestations of cartilage damage. The aim of this investigation was to show the protein changes in KBD cartilage and to identify the candidate proteins in order to understand the pathogenesis of the disease. Proteins were extracted from the media of primary cell cultures of KBD and normal chondrocytes, and separated by two-dimensional fluorescence difference gel electrophoresis (2-D DIGE). MALDI-TOF/TOF analysis revealed statistically significant differences in 27 proteins from KBD chondrocyte cultures, which consisted of 17 up-regulated and ten down-regulated proteins. The results were further validated by Western blot analysis. The proteins identified are mainly involved in cellular redox homeostasis and stress response (MnSOD, Hsp27, Peroxiredoxin-1, and Cofilin-1), glycolysis (PGK-1, PGM-1, α-enolase), and cell motility and cytoskeletal organization (Actin, Calponin-2, and Keratin). These KBD-associated proteins indicate that cytoskeletal remodeling, glycometabolism, and oxidative stress are abnormal in KBD articular cartilage.

[Detection of proinflammatory cytokine levels in sera from patients with Kaschin-Beck disease].

AIM: To explore the role of proinflammatory cytokines (TNF, IL-1beta and IL-6) in the pathogenesis of Kaschin-Beck disease (KBD). METHODS: The levels of serum TNF, IL-1beta and IL-6 from 62 KBD patients and 60 healthy persons were detected by double antibody sandwich ELISA. RESULTS: The levels of serum IL-1beta and IL-6 in KBD patients were (238.4+/-698.5) ng/L and (164.4+/-661.4) ng/L, respectively, but they were higher than those in healthy persons, being (74.5+/-130.0) ng/L and (52.2+/-154.6) ng/L, respectively. There were no significant differences between them (P>0.05). However, the level of serum TNF in KBD patients [(109.2+/-145.3) ng/L] was significantly higher than that in healthy persons [(40.9+/-89.7) ng/L] (P<0.01). Moreover, there was no correlation between serum TNF and IL-1beta levels (r=0.0387, P>0.05) and TNF and IL-6 in KBD patients (r=0.2135, P>0.05), but there was positive correlation between serum IL-1beta and IL-6 levels (r=0.346, P<0.01). CONCLUSION: The elevated proinflammatory cytokine levels in sera may relate to the pathogenesis of Kaschin-Beck disease.