| Abstract: | 本研究的目的在探討兒茶素(EGCG)在人類眼睛疾病動物模式中對於眼睛的保護功效。研究分為兩部分，第一部分探討兒茶素中的EGCG對UVB誘發小鼠角膜氧化性損傷的保護功效。研究結果顯示，相較於正常控制組而言，UVB對照組的小鼠角膜有明顯嚴重的潰瘍及損傷，證實UVB會照成角膜的損傷，同時UVB對照組的小鼠角膜組織中的抗氧化酵素活性(SOD、catalase、GSH-Px and GSH-Rd)及GSH含量顯著的降低(p< 0.05)，角膜的脂質過氧化及蛋白質氧化的指標顯著提高(p< 0.05)，證明UVB會造成角膜的氧化性損傷。另一方面，給予不同劑量EGCG眼藥水實驗組之小鼠角膜的平滑度及染色評估角膜損傷均明顯(p < 0.05)比UVB組良好，證明含有EGCG之眼藥水可以保護角膜不受UVB的傷害；另外，EGCG眼藥水可顯著(p< 0.05)提高角膜組織中抗氧化酵素的活性及增加GSH的含量，同時也有顯著(p< 0.05)降低角膜的脂質過氧化及蛋白質氧化傷害。綜合以上結果證明EGCG眼藥水具有保護或緩解UVB所誘發之小鼠角膜氧化損傷之能力。第二部分是探討兒茶素EGCG對亞硒酸鈉誘發大鼠仔鼠白內障及氧化傷害的保護功效。實驗結果顯示，亞硒酸鈉對照組的仔鼠水晶體比正常控制組有明顯嚴重的核性白內障的產生，證實亞硒酸鈉會誘發白內障的產生。在給予不同劑量EGCG實驗組的仔鼠水晶體的混濁程度均明顯(p< 0.05)比亞硒酸鈉組降低，證明EGCG可以保護水晶體延緩亞硒酸鈉誘發白內障的產生。另外，EGCG可顯著(p< 0.05)提高水晶體組織中抗氧化酵素的活性及增加GSH的含量，同時也具有顯著(p< 0.05)降低亞硒酸鈉引起的蛋白質氧化傷害。綜合結果顯示，EGCG具有保護或緩解亞硒酸鈉所誘發之仔鼠水晶體混濁及氧化損傷之能力。
The aim of this study was to evaluate the functional activities of (-)-epigallocatechin gallate on animal models for human eye diseases. The first part of present study was to investigate the protective effects of epigallocatechin gallate (EGCG) on UVB radiation–induced corneal oxidative damage in mice. The results indicated that UVB radiation caused significant damage to the corneas, including apparent corneal ulceration and severe epithelial exfoliation, leading to a decrease in SOD, catalase, GSH-Px, GSH-Rd, and GSH activity in the cornea. However, the corneal TBARS and protein carbonyls increased comparing with the control group. Treatment with EGCG eye drops significantly (p<0.05) ameliorated corneal damage, increased SOD, catalase, GSH-Px, GSH-Rd, and GSH activity, and decreased the TBARS and protein carbonyls in the corneas compared with the UVB-treated group. Taken together, EGCG eye drops exhibit potent protective effects on UVB radiation–induced corneal oxidative damage in mice. The second part of the present study was to evaluate the protective effects of EGCG on sodium selenite-induced cataractogenesis in rat pups. The results demonstrated that sodium selenite caused significant (p < 0.05) cataract formation, a reduction of the activities of SOD, catalase, and GSH level, and an increase of protein carbonyls level comparing with the normal control group. In contrast, treatment with EGCG could significantly (p < 0.05) ameliorate cataract formation and oxidative damage in the lens. Moreover, EGCG administration significantly increased the GSH level and the activities of SOD and catalase, and declined the protein carbonyls in the lens when it compared with the sodium selenite group. Taken together, EGCG administrations demonstrate effective protective effects on sodium selenite-induced cataract and oxidative injury in rat pups. |
