方法：建立高糖诱导的HLEC氧化损伤模型，用不同浓度的EGCG干预，MTT检测细胞活力，倒置显微镜观察细胞形态，Hoechst-PI染色观察细胞凋亡，分光光度计检测上清液中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)及丙二醛(MDA)的含量。

结果：MTT结果显示用10μmol/L EGCG和100μmol/L EGCG处理后，HLEC活性分别提高到50.33%±3.52%和63.33%±4.63%，与氧化损伤组(32.67%±3.10%)比较差异具有统计学意义(P<0.05)； EGCG干预的高糖条件下的HLEC较好地保持了细胞的形态，凋亡细胞数量减少，细胞内SOD、GSH-Px水平升高，MDA水平下降。

结论：EGCG可能通过提高细胞内SOD、GSH-Px含量，降低MDA含量发挥其较强的抗氧化作用，从而为寻求有效的防治白内障药物提供可靠的实验依据。

METHODS: The HLE cell oxidative damage model induced by high concentration glucose was established, and was intervented with different concentrations of EGCG. Cell viability was determined by MTT assay, cell morphology was investigated by convert microscope, cells apoptosis was assayed by flow cytometry with Hoechst-PI staining. Moreover, the levels of super oxide dismutase(SOD), glutathione peroxidase(GSH-Px)and malondialdehyde(MDA)in supernatant were also tested after different treatment either with high concentration glucose or with different concentrations of EGCG.

RESULTS: MTT results showed that HLE cells activity increased to 50.33%±3.52% and 63.33%±4.63% after treated with 10 μmol/L and 100 μmol/L EGCG respectively, the difference was statistically significant compared with oxidative injury group(32.67%±3.10%)(P<0.05); HLE cells maintained better morphology intervented with EGCG under high glucose conditions, the number of apoptotic cells reduced, SOD and GSH-Px level within HLE cells increased and MDA levels decreased.

CONCLUSION: EGCG plays its strong antioxidant effect by increasing SOD, GSH-Px content and decreasing MDA content in cells, therefore provides a reliable experimental basis for the search for effective prevention and treatment of cataract drug.