Oleanolic acid prevents cartilage degeneration in diabetic mice via PPARγ associated mitochondrial stabilization
Oleanolic acid prevents cartilage degeneration in diabetic mice via PPARγ associated mitochondrial stabilization
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DOI：
10.1016/j.bbrc.2017.06.127
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发表时间：
2017-08-26
影响因子：
3.1
通讯作者：
Chen, Ken
中科院分区：
文献类型：
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作者：
Kang, Xia;Yang, Zhikui;Chen, Ken
高血糖诱导的软骨退变诱导骨关节炎（OA）。由于油酸（奥拉）具有抗炎、抗氧化等药理作用，我们推测其对高糖损伤的软骨具有保护作用。我们现在报告说，奥拉减少了X型胶原蛋白并逆转了db/db小鼠生长板中的软骨变性。奥拉以浓度依赖性方式（10-50 μ M）增加高糖处理的软骨细胞中II型胶原的表达。奥拉可抑制高糖诱导的细胞损伤，并通过降低线粒体膜电位降低MMP-13、PGE 2和IL-6的水平，刺激ATP的产生。此外，奥拉处理抑制细胞凋亡。SOD 2表达和活性的逆转可能是由于奥拉处理通过PPPA γ降低了SOD 2蛋白的降解。结论：奥拉通过过氧化物酶体增殖物激活受体γ/超氧化物歧化酶2途径对高糖诱导的软骨损伤具有保护作用。(C)2017爱思唯尔公司All rights reserved.
Hyperglycemia-induced cartilage degeneration induces osteoarthritis (OA). Since oleanolic acid (OLA) have several pharmacological effects such as anti-inflammatory, anti-oxidant, we hypothesized it possesses protection against high glucose injured cartilage. We now report that OLA decreased type X collagen and reversed the cartilage degeneration in growth plate from db/db mice. OLA increased type II collagen expression in a concentration-dependent manner (10-50 mu M) in high glucose-treated chondrocytes. OLA prevented the high glucose induced cell injury and decreased the level of MMP-13, PGE2 and IL-6 due to decreasing mitochondrial membrane potential and stimulated the ATP production. Moreover, OLA treatment inhibited apoptosis. And the reversed SOD2 expression and activity may be ascribed to decreased SOD2 protein degradation by OLA treatment, via PPPA gamma. In conclusion, OLA protected against the high-glucose-induced cartilage injury via PPAR gamma/SOD2 pathway. (C) 2017 Elsevier Inc. All rights reserved.