Abstract
High fluence low-power laser irradiation (LPLI) can induce cell apoptosis which is mediated by a high level of mitochondrial reactive oxygen species (ROS) production; however the mechanism is still unclear. Here, we further studied the mitochondrial signaling pathways involved in the apoptotic process. Activation of caspase-9 indicated an apoptotic process occurred under the high fluence LPLI treatment. Increasing of dichlorodihydrofluorescein diacetate (H 2 DCFDA) fluorescence products showed a high level of mitochondrial ROS generation after irradiation. Cyclosporine A (CsA) has been reported to inhibit some kinds of apoptosis, which are especially mediated by ROS. The question is whether CsA has some effect on high fluence LPLI induced apoptosis. Results showed that CsA significantly delayed mitochondria depolarization, observably delayed cell death in response to high fluence LPLI treatment demonstrating a significant protective role of CsA on the apoptotic process. These results suggest that high fluence LPLI induced cell apoptosis via some CsA-sensitive mitochondrial signal pathways.
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