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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: AIP1 suppresses neovascularization by inhibiting the NOX4-induced NLRP3/NLRP6 imbalance in a murine corneal alkali burn model

Fig. 4

The NOX4 inhibitor GLX351322 reverses the imbalance in NLRP3 activation and NLRP6 suppression. A Representative slit-lamp images revealing that GLX351322 eye drops notably decreased neovascularization compared with that in the control group (magnification: × 40). B Corneal whole-mount staining revealed that GLX351322 eye drops notably decreased neovascularization compared with that in the control group (scale bar: 1 mm). C The corneal opacity, neovessel size, and vessel size scores decreased significantly in the GLX351322 eye drop groups compared with those in the control groups after alkali burn injury (N = nine). D The DCFDA ROS assay revealed that GLX351322 eye drops significantly reduced the increase in ROS induced by alkali burn injury compared with that in the control group (scale bar: 100 μm). E RT–qPCR showed that GLX351322 eye drops significantly abrogated the reduction in NLRP6 and decreased the elevation in NLRP3 and VEGFa induced by alkali burn injury (N = three). F Western blot analysis showed that GLX351322 eye drops significantly abrogated the reduction in NLRP6 and decreased the elevation in NLRP3, ASC, clv-casp1 and clv-IL-1β induced by alkali burn injury (N = three). The error bars represent the mean ± SD, and comparisons were performed using one-way ANOVA. clv-casp1, cleaved caspase-1; clv-IL-1β, cleaved-IL-1β. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

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