Disturbance of nivalenol on expression of adhesion molecule CD44 on surface of cultured chondrocytes

Background: Deficit of nivalenol (NIV) and selenium (Se) is related with kashin-beck disease (KBD) to certain extent. Hyaluronic acid (HA) metabolism affects directly the polymerization of proteoglycans (PG) and normal structure and function of cartilage. The integration with HA receptor on surface of cartilage tissue is the key link in HA metabolism. Being the main receptor of HA on chondrocytic membrane, CD44 expression impacts directly HA metabolism, further affects cartilage matrix metabolism, which is extremely important to maintaining the structure and function of cartilage matrix. Objective: To probe into the injury and protection of related etiology of KBD to target tissue cells and the mechanism on degenerative necrosis of chondrocytes. Design: Randomized controlled observation was designed. Setting: Department of Genetics and Molecular-Biology of Medical College of Xi'an Jiaotong University. Materials: The experiment was performed in Key Laboratory Room on Ministry of Education associated with Environment and Disease of Xian Jiaotong University from October 2002 to July 2004. One New Zealand pedigree young rabbit aged 30 days was employed and its humerus, femurs and tibia were cut out in surgery. Methods: With cell culture, the model of bone tissue was reconstructed in vitro, in which, NIV of various concentrations, KBD suspicious infectious agent and Se, the protective factor were added. HA receptor CD44 on chondrocytic membrane and soluble CD44 in cell culture solution were determined. Main outcome measures: 1 Microscopic observation of adhesion molecule CD44 on chondrocytic surface. 2 Soluble CD44 in chongrocytic culture solution. Results: 1 Microscopic observation of adhesion molecule CD44 on chondrocytic surface: CD expression in chondrocytic membrane was decreased with increasing of NIV concentration and it was in tendency of increasing with Se added. 2 Soluble CD44 in chongrocytic culture solution: The concentration of soluble CD44 in cell culture solution was decreased gradually following the increased concentration of NIV, but it was increased in high concentration group and such tendency did not alter when Se added. Except blank control and Se control, significant difference was presented among groups (P < 0.05). Conclusion: NIV disturbs adhesion molecule CD44 expression on chondrocytic surface and further induces metabolic disturbance of cartilage extracellular matrix. Se supplementation can resist the injury of NIV to chondrocytes, but its action is limited.