Effect of type II diabetes-induced osteoarthritis on articular cartilage aging in rats: A study in vivo and in vitro

Some evidence suggests that type II diabetes mellitus (T2DM) and osteoarthritis (OA) usually occur together clinically, and the symptoms are more obvious compared with non-diabetic patients with OA. We aimed to explore the effects in cartilage degradation, damage, and aging after T2DM combined with OA. Thirty male Sprague-Dawley (SD) rats were randomly divided into the young-control group (YCG, n = 10), old-control group (OCG, n = 10), and old T2DM-induced OA group (OTOG, n = 10) after the pre-experiment. T2DM model was established using a high-fat diet and streptozotocin. In vivo, all rats were evaluated by behavior, histology, immunohistochemistry, and enzyme-linked immunosorbent assay (ELISA). In vitro, chondrocytes of 17-day-old SD rats were cultured to obtain the passage 1 (P1) and passage 5 (P5) chondrocytes. The effects of different concentrations glucose on chondrocyte senescence were evaluated by chondrocyte staining, immunofluorescence, western blotting, and ROS analysis. The results of histology (hematoxylin-eosin staining, safranin O-fast green staining, alizarin red S staining, and Mankin score), immunohistochemistry (COL-II, MMP-13, and p21), ELISA (IL-6 and IL-8), western blotting (COL-II, MMP-13, p21, p53, and p16), immunofluorescence, and ROS analysis indicated that the degeneration and aging in the articular cartilage of OTOG were more serious than other groups. Moreover, high concentration glucose can accelerated the degradation and aging degree of cartilage. The changes in P5 are more obvious than in P1 cells. T2DM-induced OA can aggravate the aging of articular cartilage in aging individuals. High concentration glucose can cause a certain degree of damage, degradation, and aging of chondrocytes.