Locostatin is a potent and cell permeable inhibitor of Raf kinase inhibitor protein (RKIP)/Raf1 kinase interaction and an inhibitor of cell migration.

Locostatin处理激活了丝裂原活化蛋白激酶（MAPK）信号通路（ERK磷酸化），为我们的靶向方案提供了有力的验证。此外，Locostatin通过抑制RKIP减少了细胞外基质（ECM）组分。同时，Locostatin对RKIP的抑制在子宫平滑肌瘤和子宫肌细胞中阻碍了细胞增殖和迁移。最终，Locostatin处理降低了GSK3β表达。因此，尽管MAPK途径的激活本应增加增殖和迁移，GSK3β的不稳定导致了子宫肌和平滑肌瘤细胞增殖和迁移的减少[1]。

与CCl4组相比，接受locostatin处理的组织中，HYP (208.56 ± 6.12) μg/g，整体区域内总胶原的百分比(1.91 ± 0.13)，MMP-13/TIMP-1(0.19 ± 0.01)，MPO (1.45 ± 0.04) U/g，TGF-β (2652 ± 91.20)，PDGF-AA (3897 ± 290.69)以及E-selectin (1569 ± 66.48) 在肝组织中的水平均显示出显著下降[2]。

Carbon tetrachloride (CCl4) was used to induce liver fibrosis in mice, and locostatin was injected intraperitoneally. Liver fibrosis was assessed by Masson and Sirius red staining, hydroxyproline (HYP) assay, and collagen percentage area. Collagen I, collagen III, and α-SMA were detected by RT-PCR and western blot. The levels of MMP-13, MMP-2, TIMP-1, and TIMP-2 were estimated by ELISA. Liver inflammation was evaluated by HE staining and immunohistochemistry; liver myeloperoxidase (MPO), superoxide dismutase, and malondialdehyde were measured by ELISA; and cytokines were by Mouse Cytokine Array Q4000[2]