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齐墩果酸通过与PPARγ相关的线粒体稳定作用预防糖尿病小鼠的软骨退变。

Oleanolic acid prevents cartilage degeneration in diabetic mice via PPARγ associated mitochondrial stabilization.

作者信息

Kang Xia, Yang Zhikui, Sheng Jun, Liu Jin-Biao, Xie Qing-Yun, Zheng Wei, Chen Ken

机构信息

Department of Orthopedics, Chengdu Military General Hospital, 270 Rongdu Avenue, Jinniu District, Chengdu, Sichuan 610083, China.

Department of Orthopedics, Xianyang Hospital of Yan'an University, 38 Wenlin Road, Xianyang, Shaanxi Province 712000, China.

出版信息

Biochem Biophys Res Commun. 2017 Aug 26;490(3):834-840. doi: 10.1016/j.bbrc.2017.06.127. Epub 2017 Jun 21.

Abstract

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 μΜ) 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 PPPAγ. In conclusion, OLA protected against the high-glucose-induced cartilage injury via PPARγ/SOD2 pathway.

摘要

高血糖诱导的软骨退变会引发骨关节炎(OA)。由于齐墩果酸(OLA)具有多种药理作用,如抗炎、抗氧化,我们推测它对高糖损伤的软骨具有保护作用。我们现在报告,OLA降低了X型胶原蛋白水平,并逆转了db/db小鼠生长板中的软骨退变。在高糖处理的软骨细胞中,OLA以浓度依赖的方式(10 - 50μΜ)增加Ⅱ型胶原蛋白的表达。OLA预防了高糖诱导的细胞损伤,并由于线粒体膜电位降低而降低了MMP - 13、PGE2和IL - 6的水平,并刺激了ATP的产生。此外,OLA处理抑制了细胞凋亡。而SOD2表达和活性的逆转可能归因于OLA通过PPPAγ处理减少了SOD2蛋白的降解。总之,OLA通过PPARγ/SOD2途径保护软骨免受高糖诱导的损伤。

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