Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Exp Gerontol. 2021 Jul 15;150:111354. doi: 10.1016/j.exger.2021.111354. Epub 2021 Apr 16.
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.
有证据表明，2 型糖尿病（T2DM）和骨关节炎（OA）在临床上通常同时发生，且症状比非糖尿病 OA 患者更为明显。我们旨在探讨 T2DM 合并 OA 后对软骨降解、损伤和老化的影响。
30 只雄性 Sprague-Dawley（SD）大鼠经预实验后，随机分为青年对照组（YCG，n=10）、老年对照组（OCG，n=10）和老年 T2DM 诱导 OA 组（OTOG，n=10）。采用高脂饮食联合链脲佐菌素建立 T2DM 模型。体内实验中，所有大鼠均进行行为学、组织学、免疫组化和酶联免疫吸附测定（ELISA）评估。体外实验中，培养 17 日龄 SD 大鼠软骨细胞，获得第 1 代（P1）和第 5 代（P5）软骨细胞。通过软骨细胞染色、免疫荧光、Western blot 和 ROS 分析评估不同浓度葡萄糖对软骨细胞衰老的影响。
组织学（苏木精-伊红染色、番红 O-快绿染色、茜素红 S 染色和 Mankin 评分）、免疫组化（COL-II、MMP-13 和 p21）、ELISA（IL-6 和 IL-8）、Western blot（COL-II、MMP-13、p21、p53 和 p16）、免疫荧光和 ROS 分析结果表明，OTOG 关节软骨的退变和老化比其他组更严重。此外，高浓度葡萄糖可加速软骨的降解和老化程度。P5 细胞的变化比 P1 细胞更明显。
T2DM 诱导的 OA 可加重老龄个体关节软骨的老化。高浓度葡萄糖可引起一定程度的软骨细胞损伤、降解和老化。
