[The Effect of Disordered Glycometabolism of Kashin-Beck Disease on the Function of Chondrocytes].

OBJECTIVE: To reveal the effect of disordered glycometabolism in Kashin-Beck disease (KBD) chondrocytes,we compared changes in expressions of extracellular matrix components (collagen and aggrecan),apoptosis and oxidative stress under the condition of different concentrations of glucose. METHODS: The damage of KBD chondrocytes and normal chondrocytes under high glucose culture was measured in compared with cells under normal culture,that included the changes of proliferation and morphology; the concentrations of glucose in culture medium during the process of chondrocytes culture; the expressions of type Ⅱ collagen and aggrecan detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Toluidine blue staining; cell apoptosis and reactive oxygen species (ROS) content detected by flow cytometry and fluorescence staining. RESULTS: The growth and proliferation of KBD chondrocytes were inferior to normal chondrocytes. The glucose uptake of KBD chondrocytes and normal chondrocytes under high glucose culture were basically the same (P>0.05). Disordered glycometabolism caused by high glucose decreased the expression of type Ⅱ collagen and aggrecan in KBD chondrocytes (P<0.05),meanwhile,increased apoptosis and cellular ROS generation of cultured chondrocytes (P<0.05). CONCLUSION: The disordered glycometabolism can affect the function of KBD chondrocytes through reducing the expression of type Ⅱ collagen and aggrecan and increasing the apoptosis and the oxidative stress.

Expression profiles of genes involved in apoptosis and selenium metabolism in articular cartilage of patients with Kashin-Beck osteoarthritis.

Kashin-Beck disease (KBD) is a special type of endemic osteoarthritis. It has been suggested that alterations in selenium metabolism and apoptosis play a role in KBD. However, the underlying molecular mechanism remains largely unclear. We performed a microarray analysis using RNA isolated from cartilages of KBD patients and healthy controls, through Significance Analysis of Microarray (SAM) software. Functional gene networks and crucial molecules associated with differentially expressed genes were investigated via Ingenuity Pathway Analysis (IPA) and hub gene analysis. Quantitative real-time PCR was used to check the validation of chip test. We identified 52 up-regulated apoptosis-related genes and 26 down-regulated selenium-related genes between KBD and controls, and these genes associated with the "MYC-mediated apoptosis signaling pathway". We confirmed the results from array studies with quantitative real-time PCR analysis. Our results suggest that abnormal regulation of selenium metabolism and apoptosis through the MYC mediated signaling pathway contributes to the pathogenesis of KBD, but the relationship between apoptosis gene and selenium gene was not found.

Ruthenium-catalyzed annulation of alkynes with amides via formyl translocation.

The first example of Ru-catalyzed intramolecular annulation of alkynes with amides via formyl translocation has been developed, which provides an efficient approach for the synthesis of 1H-indole-3-carbaldehydes.

Copper-catalyzed intramolecular C-H oxidation/acylation of formyl-N-arylformamides leading to indoline-2,3-diones.

A new, efficient Cu-catalyzed intramolecular C-H oxidation/acylation method has been developed for the synthesis of substituted indoline-2,3-diones (isatins). In the presence of CuCl(2) and O(2), a variety of formyl-N-arylformamides underwent the tandem reaction to afford the corresponding indoline-2,3-diones in moderate to good yields. It is noteworthy that the reaction serves as the first example of transition-metal-catalyzed transformation for the preparation of indoline-2,3-diones.