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[摘要]
目的:探究核苷酸结合寡聚化结构域样受体3(NLRP3)/白介素-1β(IL-1β)通路在增殖性糖尿病视网膜病变中的作用机制。
方法:收集2015-09/2018-03我院眼科收治的增殖性糖尿病视网膜病变患者49例49眼(研究组)和特发性黄斑裂孔患者41例41眼(对照组)。检测研究组患者视网膜增殖前膜与对照组患者黄斑前膜中NLRP3蛋白表达情况、活性氧簇(ROS)、丙二醛(MDA)水平与超氧化物歧化酶(SOD)活性,测定两组患者玻璃体中IL-1β与IL-18浓度。
结果:研究组患者视网膜增殖前膜中NLRP3蛋白阳性表达率明显高于对照组患者黄斑前膜(90% vs 5%,P<0.05),且研究组患者视网膜增殖前膜中ROS与MDA水平明显升高,而SOD活性明显降低。研究组患者玻璃体中IL-1β、IL-18浓度(30.84±7.15、97.61±15.73pg/mL)均明显高于对照组(4.63±0.92、52.07±11.38pg/mL)。
结论:NLRP3与IL-1β在增殖性糖尿病视网膜病变组织中呈高表达,NLRP3/IL-1β通路可上调炎性因子与氧化因子表达水平,促进疾病发展。
[Key word]
[Abstract]
AIM: To explore the mechanism of action of nucleotide-binding oligomerization domain-like receptor 3(NLRP3)/interleukin-1β(IL-1β)pathway in proliferative diabetic retinopathy.
METHODS: Totally 49 cases(49 eyes)of proliferative diabetic retinopathy(study group)and 41 cases(41 eyes)of idiopathic macular hole(control group)in ophthalmology department of our hospital from September 2015 to March 2018 were selected. The expression of NLRP3, the levels of reactive oxygen species(ROS), malondialdehyde(MDA)and the activity of superoxide dismutase(SOD)in proliferative epiretinal membrane and macular epiretinal membrane were measured. The concentrations of IL-1β and interleukin-18(IL-18)in the vitreous of the two groups were also determined.
RESULTS: The positive expression rate of NLRP3 protein in the study group was significantly higher than that in the control group(90% vs 5%, P<0.05). The concentration of IL-1β and IL-18 in the vitreous of the study group was significantly higher than that in the control group \〖(30.84±7.15)vs(4.63±0.92);(97.61±15.73)pg/mL vs(52.07±11.38)pg/mL, P<0.05\〗. The levels of ROS and MDA of the study group were significantly higher than those of the control group(P<0.05). The activity of SOD in the retina of the study group was significantly lower than that of the control group(P<0.05).
CONCLUSION: NLRP3 and IL-1β are highly expressed in proliferative diabetic retinopathy. The NLRP3/IL-1β pathway can up-regulate the expression levels of inflammatory and oxidative factors and promote disease progression.
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