Fig 9. bFGF reverses the high glucose-induced impairment of VEC migration by suppressing ROS accumulation due to activation of JNK and ERK.

High glucose was used to simulate hyperglycemia in vivo. Hyperglycemia obviously upregulates phosphorylation of JNK and ERK, and the activated forms of these two MAPKs cause accumulation of intracellular ROS, resulting in impairment of cell migration. bFGF treatment of cells incubated in high-glucose media indirectly inhibits the abnormal activation of MAPKs via its signaling pathway, reducing the accumulation of ROS and preventing the delay in cell migration.