Abstract:Objective To investigate the mechanism of inflammation promoting lymphatic growth. Methods BALB/c mice were sutured to simulate the inflammatory process. The expression of nuclear factor kappa-B (NF-κB) in physiological and inflammatory lymphatic endothelium was located by corneal frozen section and immunofluorescence staining. Then, the protein expression of NF-κB in corneal tissue was quantitatively analyzed by Western blot. The inflammatory model mice were subcutaneously injected with MG-132, a specific proteasome inhibitor of NF-κB, after operation, and the mice were divided into treatment group (n=10) and control group (n=10) according to whether they were injected or not. The expression of Ang-2 mRNA in cornea of the two groups was detected by reverse transcription fluorescence quantitative PCR, and the growth of lymphatic vessels of the two groups was compared by HE staining and immunohistochemical staining. Results Immunofluorescence staining showed that the expression of NF-κB in inflammatory lymphatic endothelial cells was higher than that in physiological lymphatic. Compared with normal mouse corneal stroma, the expression level of NF-κB protein in inflammatory cornea was higher. The expression of Ang-2 mRNA in MG-132 treatment group reached the peak on the first day after injection, and then decreased gradually, while the expression level of Ang-2 mRNA in control group increased gradually (P＜0.01). In normal cornea, lymphatic vessels grew only in the limbal. Fourteen days after MG-132 injection, compared with the control group, the number of lymphatic vessels in the treatment group were significantly reduced (P＜0.01) and the diameter of lymphatic ressels was smaller. Conclusion In inflammatory environment, NF-κB is the promoter of Ang-2. Its up-regulated expression induces the increase of Ang-2 protein synthesis, and finally stimulates and promotes the growth of inflammatory lymphatic vessels.