Fig 2: Regulation of SOD1/2 and cyclin D1 proteins induced by C8-ceramide. After C8-ceramide treatment, SOD1 downregulation may be controlled by ROS, which can negative feedback to SOD1 switched SOD2 and then modulated the expression of cyclin D1. ß-actin as an internal control.

Fig 3: A proposed model of C8-ceramide-induced apoptosis and anti-proliferation of non-small-cell lung cancer cells by modulating the differential expressions of superoxide dismutases and cell cycle G1 arrest. After C8-ceramide treatment, the SOD1 to SOD2 switch stimulated by ROS induces the excess accumulation of cyclin D1, a feedback loop, which in turn causes cell cycle G1 arrest. Eventually, C8-ceramide induces the growth arrest and the apoptotic cell death in lung cancer H1299 cells. The upwards arrows and downwards arrows indicate the upregulation and downregulation respectively.

Fig 4: Summary of CCL5 in GPX1 activation and neuron protection after brain injury. (A) Brain injury induces ROS generation in mouse hippocampus which can be scavenged by the SOD and GPX systems and increase neuron survival with the presence of CCL5. (B) Increased H2O2 produces hydroxyl radical (OH·) and hydroxy (OH-) through the Fenton reaction and causes hippocampal neuron death in the absence of CCL5.