Tetramethylpyrazine (TMP) ameliorates corneal neovascularization via regulating cell infiltration into cornea after alkali burn.

摘要: Abstract In the present study, we investigated underlying mechanism of tetramethylpyrazine (TMP)-medicated inhibition corneal neovascularization (CNV). Our data showed that TMP could effectively downregulate expression levels CXCR4 mRNA and protein, as well inhibit HUVECs, endothelial cells, tubule formation in vitro. vivo, alkali burn (1 M NaOH) remarkably upregulate increase migration TNF-α-positive cells to stroma. drops significantly cornea, compared control. However, there was no difference downregulation between FK506, an immunosuppressive drug. Moreover, immunofluorescent staining CD45 FK506 restrain bone marrow (BM)-derived infiltration while F4/80 reflects suppression macrophage aggregation. Meanwhile regulate Interleukin 10 (IL-10) 2 (IL-2). Furthermore, ameliorate opacity neovascularization. Clinical assessment detected obvious improvement treatment groups, controls vivo. Thus, had similar effects immune response CNV by suppressing BM-infiltrating into cornea FK506. be a potential agent eye-drop therapy for damaged Alkali Burn.