|
목적 : Pterygium is a common ocular surface disease in person and characterized by inflammatory cell infiltrates, cellular proliferation, angiogenesis and inflammation. Chronic ultraviolet B(UVB) light exposure is a causal factor in the pathogenesis of this disease, but the mechanism is not completely understood. HMGB-1(high mobility group box 1), nuclear protein that acts as a damage-associated molecular pattern after its releases by necrotic cell. We investigate the expression and amelioration of HMGB1 in UVB radiated pterygial tissue.
방법 : The conjunctiva of Balb/c mice were exposed to UVB irradiation using a UV cross linker lamp. For blocking the effect of HMGB1, mice were injected intraperitoneally with PBS, sRAGE or A-box. For inhibition of reactive oxygen species production, mice were injected intraperitoneally NAC or mitotempo. Western blot and ELISA were also conducted for the measurement of HMGB1 level in UV irradiated Chang cells, mice conjunctiva and human pterigial tissue. For the histological analysis, frozen section were done with mice conjunctiva and human pterigial tissue and examined under a confocal microscope.
결과 : We show that UVB irradiation induce mouse conjunctival inflammation through HMGB-1 which is released by conjunctiva epithelial cell. Our data also demonstrate translocation into cytoplasm and secretion into extracellular space of HMGB-1 depends on UVB induced ROS production in conjunctiva epithelial cell. Intraperitoneal administration of NAC resulted in amelioration of UVB irradiation induced conjunctival inflammation. In human pterygium tissue, epithelial cell also were shown that translocation of HMGB1 to the cytosol. Secretion of HMGB-1 were increased after UVB irradiation in conjunctiva.
결론 : Taken together, HMGB-1 is one of the critical factors in UVB induced conjunctival inflammation and human Pterygium. Moreover, it is expected be useful for further understanding of the pathogenesis of UV induced ophthalmic lesion.
|