ABSTRACT
@#Retinal degenerative diseases are kinds of leading cause of blindness characterized by photoreceptor apoptosis and progressive neuronal degeneration. A large body of research has shown the evidence of inflammation reaction in such diseases. Retinal neuroinflammation may be a main factor resulting in apoptosis of photoreceptors and neurodegeneration of retina. In addition, the inflammatory response is not only detected in the retina, but also in aqueous humor, vitreous and even in blood, which forms a persistently very low degree, and chronic inflammatory environment. In this review, we focus on the development of microinflammatory response and its predictor for disease outcomes.
ABSTRACT
Abstract?AIM: To investigate mechanism of bradykinin ( BK) on inflammations of retinal pigment epithelium ( RPE) cells.?METHODS: ARPE -19 cells were cultured in vitro, stimulated by 100nM BK for 24h. Cell morphology changes were observed by microscope, and BK receptor localization was detected through cell immunofluorescence. Changes of Ca2+in BK and BR antagonist stimuli were detected by laser scanning confocal microscopy.The expressions of COX-1, COX-2, eNOS and iNOS protein in control group and BK group were detected by Western Blot.?RESULTS: After the stimulation of BK, there was no significant changes of ARPE-19 cells in morphology.Kinin B1 receptors ( B1R ) and B2 receptors ( B2R ) could be detected in ARPE-19 cells.Compared with control group, Ca2+concentrations significantly increased in BK group; in B1R antagonist group and B2R antagonist group Ca2+concentrations increased less than BK group; B1R and B2R antagonist group showed no obvious changes in Ca2+concentrations.Compared with control group, COX-2 and iNOS protein concentrations were significantly increased in BK group (P<0.001).?CONCLUSION:BK induces the increasing expression of COX-2 and iNOS in the cultured ARPE cells through binding with either B1R or B2R.