Fundamental & clinical pharmacology
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Fundam Clin Pharmacol · Feb 2015
Advanced glycation end products-induced chondrocyte apoptosis through mitochondrial dysfunction in cultured rabbit chondrocyte.
Advanced glycation end products (AGEs) are an important mediator in osteoarthritis (OA) and cause apoptosis in articular chondrocytes. Mitochondrial function is involved in modulating apoptosis of articular chondrocytes. This study was performed to investigate the mechanism of AGEs-induced chondrocyte apoptosis. ⋯ We found that AGEs induced apoptosis in primary rabbit chondrocytes, upregulation of ROS production, cytochrome c, and caspase-3 levels. Simultaneously, AGEs decreases the levels of ▵Ψm and ATP production; however, the antibody of AGEs (sRAGE) and antioxidant-N-acetylcys-teine (NAC) significantly reversed AGEs-induced the above damage thus to protect the cells from apoptosis. These observations suggested that the mechanism of AGEs-induced chondrocyte apoptosis was primarily via ROS production and mitochondria-mediated caspase-3 activation.
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Fundam Clin Pharmacol · Feb 2015
The determination of histopathological and biochemical effects of the rabbit knee joint injected dexketoprofen trometamol.
This study was conducted to investigate possible histopathological effects and biochemical reflections of intra-articular dexketoprofen trometamol. A total of 24 New Zealand rabbits were included in the study. Blood sampling was carried out from all animals on the first day, then they were randomly allocated either to the control group (Group C, n = 9) or the dexketoprofen trometamol group (Group D, n = 15). ⋯ Basal TNF-α levels were higher compared with day 1 in Group C1, and IL-6 and CRP levels were higher in Group D3. Also, none of the increases in these values are supported by histopathological evaluation results. Consequently, we suppose that dexketoprofen trometamol does not cause histopathological deterioration in articular cartilage of rabbits, and the increases in biochemical parameters exclusively are not clinically significant.