首页> 外文期刊>Journal of receptor and signal transduction research >Taurine exerts anti-osteoclastogenesis activity via inhibiting ROS generation, JNK phosphorylation and COX-2 expression in RAW264.7 cells
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Taurine exerts anti-osteoclastogenesis activity via inhibiting ROS generation, JNK phosphorylation and COX-2 expression in RAW264.7 cells

机译:牛磺酸通过抑制RAW264.7细胞中的ROS生成,JNK磷酸化和COX-2表达来发挥抗破骨细胞活性

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摘要

Taurine is one of the abundant amino acids present in mammalian cells. It exerts various physiological actions such as wound healing, radioprotection, neuroprotection and anti-anxiety. In the present study, we sought to determine if taurine could inhibit osteoclastogenesis and explore the potential role of cyclooxygenase-2 (COX-2) and Jun N-terminal kinase (JNK) with reactive oxygen species (ROS). The level of intracellular ROS generated by lipopolysaccharide (LPS) was measured with DCFH-DA staining and fluorescence microscopic analysis was also performed in response to taurine in RAW264.7 cells. The expression of COX-2 and phosphorylation status of JNK by LPS was analyzed by Western blot analysis in the presence of taurine. Osteoclastogenesis was induced by LPS in the absence or presence of taurine and TRAP assay was performed to confirm the formation of osteoclast cells. ROS production was significantly enhanced by LPS and taurine treatment inhibited the ROS generation in a dose-dependent manner. The fluorescence microscopic analysis clearly showed the inhibition of ROS staining by taurine. Western blot analysis indicated that taurine significantly inhibited LPS induced COX-2 protein expression and it also inhibited phosphorylation of JNK. Taurine at the same concentration inhibited osteoclastogenesis induced by LPS, suggesting that taurine prevent osteoclast differentiation by inhibiting ROS generation. Inhibition of COX-2 expression and JNK phoshorylation could be an important mechanism by which taurine exerts antiosteoclastogeneis.
机译:牛磺酸是哺乳动物细胞中存在的丰富氨基酸之一。它发挥各种生理作用,例如伤口愈合,放射防护,神经保护和抗焦虑。在本研究中,我们试图确定牛磺酸是否可以抑制破骨细胞生成,并探讨环氧合酶2(COX-2)和Jun N末端激酶(JNK)与活性氧(ROS)的潜在作用。用DCFH-DA染色法测定脂多糖(LPS)产生的细胞内ROS水平,并对RAW264.7细胞中的牛磺酸进行荧光显微镜分析。在牛磺酸存在的情况下,通过蛋白质印迹分析来分析LPS产生的COX-2的表达和JNK的磷酸化状态。在不存在或存在牛磺酸的情况下,LPS诱导破骨细胞发生,并进行TRAP分析以确认破骨细胞的形成。 LPS显着增强了ROS的产生,牛磺酸处理以剂量依赖的方式抑制了ROS的产生。荧光显微镜分析清楚地表明牛磺酸抑制了ROS染色。蛋白质印迹分析表明,牛磺酸显着抑制LPS诱导的COX-2蛋白表达,并且还抑制JNK的磷酸化。相同浓度的牛磺酸可抑制LPS诱导的破骨细胞生成,表明牛磺酸可通过抑制ROS的生成来防止破骨细胞分化。抑制COX-2表达和JNK磷酸化可能是牛磺酸发挥抗成骨作用的重要机制。

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