In normal conditions, water and ion homeostasis in retina is controlled by Muller cells via the transmembrane aquaporin water channels. Muller cells do not BKM120 944396-07-0 express GFAP under normal physiological situations. The end feet of retinal astrocytes and Muller cells wrap around the blood vessels of the superficial retina and express AQP4. GFAP up-regulation is a hallmark of astrocyte and Muller cell activation and the resulting reactive gliosis. Expression of GFAP in Muller cells and astrocytes occurs under pathological conditions such as I/R injury. In addition, over-expression of AQP4 is associated with water influx into the retina during injury. Water influx is further exaggerated during reperfusion. Swelling and hypertrophy of Muller cells occur consequently upon overloading of intracellular K + and the movement of water inside cells. It has been shown that the deletion of AQP4 gene can protect retina against swelling in a mouse model of ischemia, thus emphasizing the importance of AQP4 in water transport. In the present study, activation of GFAP and AQP4 was observed in the vehicle-treated retina, indicating the role of Muller cells and AQP4 controlling water transport in retina. Moreover, retinal swelling was noted in ischemic retina. These results indicate a close association among the BRB integrity, the control of water flux and retinal swelling. Here, we show that LBP pre-treatment could diminish the activation of GFAP and AQP4, as well as retinal swelling in retinal I/R injury, implying the inhibitory effects of LBP in retinal swelling by minimizing the activation of Muller cell and AQP4. Oxidative stress plays a role in retinal I/R injury due to the high content of polyunsaturated fatty acid in retina. Reactive oxygen species and free radical formation during I/R Palbociclib facilitates lipid peroxidation of membrane, denature of protein and DNA damage. The breakdown of DNA strands activates the nuclear enzyme poly polymerase to produce PAR. PARP cleaves nicotinamide adenine dinucleotide, and subsequently leads to energy failure and cell death. Another pathway of inducing oxidative stress is the nitrosative injury. Free radical formation facilitates nitric oxide production, which reacts with superoxide to from peroxynitrite, a strong oxidant. Peroxynitrite leads to nitration of tyrosine residues of cells to form NT. Therefore, NT is an indicator for oxidative-nitrosative stress. Increased immunoreactivity of PAR and NT was observed in the vehicle-treated I/R retina, indicating increased oxidative stress associated with retinal I/R. In addition, oxidative stress has been shown to have an injurious role in BRB integrity by disruption of tight junctions in retina. ROS generated in ischemia up-regulates vascular endothelial growth factor gene expression.