方法：以人视网膜血管内皮细胞为研究对象，建立高糖损伤模型。胃饥饿素处理细胞后，采用CCK-8试剂盒检测不同浓度胃饥饿素对高糖下细胞增殖的影响，以筛选最佳浓度。将细胞分为正常对照组(NC)、胃饥饿素组(ghrelin)、高糖组(HG)和胃饥饿素+高糖组(ghrelin+HG)。采用CCK-8试剂盒检测细胞增殖，Annexin-APC/7-AAD试剂盒检测细胞凋亡，蛋白质印迹法检测细胞NLRP3、Caspase-1、IL-1β及IL-18的表达。

结果：与NC组(100.00%±0.00%)相比，HG组细胞增殖率(69.87%±0.68%，P<0.05)明显下降。与HG组相比，ghrelin+HG组细胞增殖率(92.31%±3.62%，P<0.05)明显升高。与NC组(4.94%±0.15%)相比，HG组细胞凋亡率(28.33%±1.37%，P<0.05)明显升高。与HG组相比，ghrelin+HG组细胞凋亡率(14.24%±0.32%，P<0.05)明显降低。与NC组相比，HG组细胞表达NLRP3、Caspase-1、IL-1β及IL-18蛋白均明显升高(均P<0.05)。与HG组相比，ghrelin+HG组细胞表达NLRP3、Caspase-1、IL-1β及IL-18蛋白均明显下降(均P<0.05)。

结论：胃饥饿素能对高糖损伤的视网膜血管内皮细胞起到保护作用，可能是通过抑制NLRP3炎症小体信号通路发挥其功能。

METHODS: A hyperglycemic injury model as a research object was established on human retinal vascular endothelial cells. CCK-8 kit was used to detect the effects of ghrelin with different concentrations on cell proliferation under high glucose, so as to screen the optimal concentration of ghrelin. The cells were then divided into normal control group(NC), ghrelin group(ghrelin), high glucose group(HG)and ghrelin+ high glucose group(ghrelin+HG). Cell proliferation was detected by CCK-8 kit, apoptosis was detected by Annexin-APC/7-AAD kit, and the expressions of NLRP3, Caspase-1, IL-1β and IL-18 proteins were detected by western blotting.

RESULTS: Compared with NC group(100.00%±0.00%), the cell proliferation rate of HG group(69.87%±0.68%, P<0.05)was significantly decreased. Compared with HG group, the cell proliferation rate of ghrelin + HG group was significantly increased(92.31%±3.62%, P<0.05). Compared with NC group(4.94%±0.15%), the cellular apoptosis rate of HG group(28.33%±1.37%, P<0.05)was significantly increased. Compared with HG group, the cellular apoptosis rate of ghrelin+HG group(14.24%±0.32%, P<0.05)was significantly decreased. Compared with NC group, the expressions of NLRP3, Caspase-1, IL-1β and IL-18 proteins were all significantly increased(all P<0.05). Compared with HG group, the expressions of NLRP3, Caspase-1, IL-1β and IL-18 proteins in ghrelin + HG group were all significantly decreased(all P<0.05).

CONCLUSION: Ghrelin can protect retinal vascular endothelial cells damaged by high glucose, it may function by inhibiting NLRP3 inflammasome signaling pathway.