目的：探讨Mcc950对过氧化氢(H₂O₂)诱导的人视网膜色素上皮细胞(ARPE-19细胞)炎性损伤的保护作用。

方法：将ARPE-19细胞分为正常对照组、H₂O₂损伤组、单纯Mcc950给药组、Mcc950预处理+H₂O₂损伤组，采用 CCK-8法检测细胞活力并确定H₂O₂和Mcc950合适的实验浓度，ELISA法检测细胞分泌的IL-1β浓度，免疫印迹(Western blot)法检测细胞中NLRP3炎性小体相关蛋白的表达情况，TUNEL染色法观察细胞凋亡情况。

结果：细胞活力随H₂O₂刺激浓度的增加逐渐下降，H₂O₂浓度为400μmol/L时细胞活力显著降低； 而0.1、1μmol/L Mcc950对细胞活力无显著影响，故选取400μmol/L H₂O₂和1μmol/L Mcc950作为合适的实验浓度。与正常对照组相比，H₂O₂损伤组细胞活力显著降低，细胞上清液中IL-1β浓度显著升高，细胞凋亡率明显增加，差异均有统计学意义(P<0.05)，而与H₂O₂损伤组比较，Mcc950预处理+H₂O₂损伤组细胞活力明显升高，细胞上清液中IL-1β浓度和细胞凋亡率均降低，差异均有统计学意义(P<0.05)。Western blot检测结果显示，H₂O₂能够促进细胞中NLRP3、Pro-caspase1和caspase1的表达，而Mcc950预处理+H₂O₂损伤组细胞中NLRP3、Pro-caspase1依然保持高表达，但caspase1表达水平得到明显抑制，表明Mcc950能有效抑制NLRP3炎性小体的激活从而干扰具有细胞凋亡作用的成熟caspase1的产生。

结论：Mcc950能够有效抑制H₂O₂诱导的NLRP3炎性小体激活，恢复细胞活力，抑制细胞凋亡。

METHODS: Cultured cell line ARPE-19 was divided into control group, H₂O₂ treating group, Mcc950 treating group and Mcc950+H₂O₂ treating group. Different concentrations of H₂O₂ and Mcc950 were used to treat the cells. Cell activity was detected by using CKK8 and proper experimental concentration of H₂O₂ and Mcc950 were determined. After the treatment, the concentration of IL-1β were detected by using ELISA. The change of NLRP3 related proteins were detected by Western blot. And cell apoptosis was examined by TUNEL stain.

RESULTS: Cell ability was gradually decreased along with the increasing treating concentrations of H₂O₂. Cell ability showed statistical difference when the concentration of H₂O₂ arrived 400μmol/L. With the concentration of 0.1 and 1μmol/L, Mcc950 had no effect on cell ability. So we chose 400μmol/L H₂O₂ and 1μmol/L Mcc950 as the experimental concentrations. Compared with the normal control group, the cell viability in the H₂O₂ treating group was significantly reduced, the IL-1β in the supernatant was significantly increased, and the apoptosis rate was significantly increased, with statistically significant differences(P<0.05). In Mcc950+H₂O₂ treating group, cell viability was significantly increased, the IL-1β in the supernatant and the apoptosis rate were significantly decreased(P<0.05). By Western blot, after treated with 400μmol/L H₂O₂, the IL-1β, NLRP3, pro-caspase1 and caspase1 were obviously increased compared to control group. After treated with Mcc950, the NLRP3 and pro-caspase1 still were at high level, the expression of caspase1 was suppressed, which indicated that Mcc950 effectively inhibited the activation of NLRP3 inflammasome consequently disturbed the formation of caspase1.

CONCLUSION: Mcc950 can inhibits the function of NLRP3, leading to increasing of the cell ability and decreasing of the cell apoptosis.