CAJ | 학술논문

青光眼是一种多因素诱导的视神经退行性病变,其中氧化应激损伤在复杂的青光眼发病机制中的起着重要作用.青光眼的氧化损伤机制可能对眼部的某些组织细胞产生损伤作用,促使细胞内抗氧化物酶作用下降、抗氧化作用相关蛋白增加,最终导致蛋白沉积、细胞死亡.氧化损伤可以导致小梁网细胞线粒体骨架改变,最终使小梁网发生退行性病理改变.氧化损伤还可促使视网膜神经节细胞内抗氧化作用相关蛋白增加、线粒体内源性凋亡,最终导致视网膜神经节细胞功能丧失.
청광안시일충다인소유도적시신경퇴행성병변,기중양화응격손상재복잡적청광안발병궤제중적기착중요작용.청광안적양화손상궤제가능대안부적모사조직세포산생손상작용,촉사세포내항양화물매작용하강、항양화작용상관단백증가,최종도치단백침적、세포사망.양화손상가이도치소량망세포선립체골가개변,최종사소량망발생퇴행성병리개변.양화손상환가촉사시망막신경절세포내항양화작용상관단백증가、선립체내원성조망,최종도치시망막신경절세포공능상실.
Glaucoma is an irreversible neuropathy and oxidative stress probably plays an important role in its pathological process.Oxidative damage can destroy cells of many parts of ocular tissue,induce decrease of intracellular antioxidant enzymes and increase antioxidant-related proteins,finally lead to deposition of these proteins and cell death.Oxidative damage also modifies the cytoskeleton of mitochondria in trabecular meshwork cells and causes pathologic degradation of trabecular meshwork cells.Oxidative stress also induces raise of antioxidant-related proteins and endogenous apoptosis of mitochondria in retinal ganglion cells,and lastly results in retinal ganglion cell dysfunction.