Y Li1, Y Zhang2, C Chen3, H Zhang4, C Ma5, Y Xia6. 1. The 163rd Central Hospital of the People's Liberation Army, The Second Affiliated Hospital of Hunan Normal University, PR China. Electronic address: feelyuqing@hotmail.com. 2. The 163rd Central Hospital of the People's Liberation Army, The Second Affiliated Hospital of Hunan Normal University, PR China. Electronic address: 66812576@qq.com. 3. The 163rd Central Hospital of the People's Liberation Army, The Second Affiliated Hospital of Hunan Normal University, PR China. Electronic address: jc163yy@163.com. 4. The 163rd Central Hospital of the People's Liberation Army, The Second Affiliated Hospital of Hunan Normal University, PR China. Electronic address: hnzhanghaibin@gmail.com. 5. The 163rd Central Hospital of the People's Liberation Army, The Second Affiliated Hospital of Hunan Normal University, PR China. Electronic address: machidoctor@126.com. 6. The 163rd Central Hospital of the People's Liberation Army, The Second Affiliated Hospital of Hunan Normal University, PR China. Electronic address: 7739816@qq.com.
Abstract
OBJECTIVE: To investigate the role of advanced glycation end products (AGEs) in cartilage degeneration in vivo and determine the influence of the peroxisome proliferator-activated receptor-γ (PPARγ) agonist pioglitazone on AGEs-induced osteoarthritis (OA) in a rabbit model. DESIGN: Thirty-two rabbits were separated into four groups (n = 8 each) and received 500 μL of 123, 350, or 1000 mmol/L D-ribose or Phosphate buffered saline (PBS) solution administered to the right stifle joint via intra-articular injection twice a week. All the rabbits ran 500 m on treadmills every day. Another 16 rabbits were administered 1000 mmol/L D-ribose and divided into 2 groups (n = 8) that received either placebo or pioglitazone administered orally at 20 mg/kg/day. Eight weeks later, cartilage damage was evaluated macroscopically, histologically, and biochemically. RESULTS: Artificially increasing the AGEs level and exercise load resulted in cartilage damage and dose-dependent downregulation of PPARγ expression. The efficacy of pioglitazone treatment was tested in a rabbit OA model, and a clear chondroprotective effect was revealed by macro- and microscopic assessments. CONCLUSION: Elevating AGEs in rabbits can accelerate the articular cartilage degradation that occurs with physical exercise, and pioglitazone can reduce the severity of the AGEs-induced OA in a rabbit model.
OBJECTIVE: To investigate the role of advanced glycation end products (AGEs) in cartilage degeneration in vivo and determine the influence of the peroxisome proliferator-activated receptor-γ (PPARγ) agonist pioglitazone on AGEs-induced osteoarthritis (OA) in a rabbit model. DESIGN: Thirty-two rabbits were separated into four groups (n = 8 each) and received 500 μL of 123, 350, or 1000 mmol/L D-ribose or Phosphate buffered saline (PBS) solution administered to the right stifle joint via intra-articular injection twice a week. All the rabbits ran 500 m on treadmills every day. Another 16 rabbits were administered 1000 mmol/L D-ribose and divided into 2 groups (n = 8) that received either placebo or pioglitazone administered orally at 20 mg/kg/day. Eight weeks later, cartilage damage was evaluated macroscopically, histologically, and biochemically. RESULTS: Artificially increasing the AGEs level and exercise load resulted in cartilage damage and dose-dependent downregulation of PPARγ expression. The efficacy of pioglitazone treatment was tested in a rabbit OA model, and a clear chondroprotective effect was revealed by macro- and microscopic assessments. CONCLUSION: Elevating AGEs in rabbits can accelerate the articular cartilage degradation that occurs with physical exercise, and pioglitazone can reduce the severity of the AGEs-induced OA in a rabbit model.
Authors: John H Rosenberg; Vikrant Rai; Matthew F Dilisio; Todd D Sekundiak; Devendra K Agrawal Journal: Mol Cell Biochem Date: 2017-06-01 Impact factor: 3.396
Authors: Weidong Zhang; Edward W Randell; Guang Sun; Sergei Likhodii; Ming Liu; Andrew Furey; Guangju Zhai Journal: PLoS One Date: 2017-09-12 Impact factor: 3.240