目的：基于NOD样受体热蛋白结构域相关蛋白3(NLRP3)炎症小体途径，探究二氢槲皮素对形觉剥夺性近视小鼠视觉功能的影响。

方法：将C57BL/6小鼠随机分为对照组和形觉剥夺性近视模型组，形觉剥夺性近视模型组通过右眼遮盖半透明眼罩来构建形觉剥夺性近视小鼠模型。造模成功后，将形觉剥夺性近视模型组小鼠随机分为模型组、二氢槲皮素低、中、高剂量组、二氢槲皮素高剂量+NLRP3激动剂组。检测各组小鼠的屈光度及眼轴长度，试剂盒检测视网膜组织中超氧化物歧化酶(SOD)、丙二醛(MDA)的水平，RT-qPCR检测视网膜组织中NLRP3、凋亡相关斑点样蛋白(ASC)、Caspase-1、IL-1β、IL-18 mRNA的表达，Western blot检测视网膜组织中NLRP3、ASC、cleaved Caspase-1、IL-1β、IL-18蛋白的表达，TUNEL染色检测视网膜组织中细胞凋亡的情况。

结果：相较于对照组，形觉剥夺性近视模型组小鼠的屈光度降低，眼轴长度增长，SOD降低，MDA、NLRP3、ASC、Caspase-1、IL-1β、IL-18升高，视网膜组织中细胞凋亡率升高(均P<0.05)； 相较于模型组，二氢槲皮素低、中、高剂量组小鼠的屈光度升高，眼轴长度缩短，SOD升高，MDA、NLRP3、ASC、Caspase-1、IL-1β、IL-18降低，视网膜组织中细胞凋亡率降低(均P<0.05)。相较于二氢槲皮素高剂量组，二氢槲皮素高剂量+NLRP3激动剂组的屈光度降低，眼轴长度增长，SOD降低，MDA、NLRP3、ASC、Caspase-1、IL-1β、IL-18升高，视网膜组织中细胞凋亡率升高(均P<0.05)。

结论：二氢槲皮素能够通过抑制焦亡及氧化应激反应来改善形觉剥夺性近视小鼠的视觉功能，其机制可能与抑制NLRP3炎症小体有关。NLRP3激动剂能够在一定程度上抑制高剂量二氢槲皮素对形觉剥夺性近视小鼠的影响。

METHODS: The C57BL/6 mice were randomly divided into control group and form deprivation myopia model group, and the form deprivation myopia model group was constructed by covering the right eye with a translucent eye patch. After successful modeling, the mice in the model group of form deprivation myopia were randomly divided into model group, low-, medium- and high-dose dihydroquercetin groups, and high-dose dihydroquercetin + NLRP3 agonist group. The diopter and axial length of mice in each group were detected. The kit was used to detect the levels of superoxide dismutase(SOD)and malondialdehyde(MDA)in retinal tissue. RT-qPCR was used to detect the mRNA expressions of NLRP3, apoptosis-associated spot-like protein(ASC), Caspase-1, IL-1β and IL-18 in retinal tissues. Western blot was used to detect the expression of NLRP3, ASC, cleaved Caspase-1, IL-1β and IL-18 proteins in retinal tissues. TUNEL staining was used to detect apoptosis in retinal tissue.

RESULTS: Compared with the control group, the diopter of the mice in the model group decreased, and axial length increased, and the SOD decreased whereas MDA, NLRP3, ASC, Caspase-1, IL-1β, IL-18 increased, and the rate of apoptosis in retinal tissue increased(all P<0.05). Compared with the model group, the diopter of mice in the low-, medium- and high-dose dihydroquercetin groups increased, axial length shortened, the SOD increased, whereas MDA, NLRP3, ASC, Caspase-1, IL-1β, IL-18 decreased, and the rate of apoptosis in retinal tissue decreased(all P<0.05). Compared with the high-dose dihydroquercetin group, the high-dose dihydroquercetin+NLRP3 agonist group had reduced diopter, increased axial length, decreased SOD levels, elevated MDA, NLRP3, ASC, Caspase-1, IL-1β, and IL-18 levels, as well as increased apoptosis rate in retinal tissue(all P<0.05).

CONCLUSION: Dihydroquercetin can improve visual function in mice with form deprivation myopia by inhibiting pyroptosis and oxidative stress responses, which may be related to the suppression of NLRP3 inflammasome. NLRP3 agonists can partially mitigate the effects of high-dose dihydroquercetin on form deprivation myopia in mice.