G protein-coupled receptor (GPCR) agonists through their receptors can transactivate protein tyrosine kinase receptors such as epidermal growth factor receptor and serine/threonine kinase receptors most notably transforming growth factor (TGF)-β receptor (TβRI). Several GPCR agonists such as Ang II, thrombin, ET‐1 can mediate the transactivation of a multitude of protein tyrosine kinase receptors[3]. Sodium ferulate (SF), a sodium salt of ferulic acid (3-methoxy-4-hydroxy-cinnamate sodium), acts as a potent antioxidant by scavenging ROS and enhancing the cell stress response through the upregulation of cytoprotective systems, such as heme oxygenase-1, superoxide dismutase, catalase, and Hsp70[4]. SF inhibits the expression and/or activity of enzymes, including inducible nitric oxide synthase, caspases, and cyclooxygenase-2, as well as the activation of JNK. In a vitro study, with treatments of 250, 500 and 1,000 μmol/l SF, the apoptotic percentage of OA chondrocytes was attenuated in a concentration-dependent manner[5]. The MCF-7 cells were treated with ferulic acid at 1 µM, 10 µM and 100 µM along with 100 ng EGF/ml from 24 to 96 h. Ferulic acid gave 14 to 30% inhibition from 24 to 96 h at 10 µM and 20 to 35% inhibition from 24 to 96 h at 100 µM[6]. In a vivo experiment, oral administration of taurine and SF (40 and 30 mg/kg/day, respectively) significantly attenuated the developed liver damage induced by administration of iron, resulting in decreases of liver weight/body weight and serum ALT and AST levels[7].
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