Tanshinone IIA Promotes the Proliferation and Migration of Schwann Cells by Regulating the PI3K/AKT Signaling Pathway.

Abstract

Introduction: To investigate the effect of tanshinone IIA on Schwann cells and its mechanisms to provide a novel approach to promote neural regeneration.

Methods: Schwann cells in the logarithmic growth phase were allocated into four experimental groups: a control group (untreated), a Tanshinone IIA (TIIA) group (20 µmol/L), a TIIA+IGF-1 group (20 µmol/L TIIA+100 ng/ml IGF-1, a PI3K/AKT pathway activator), and a TIIA+LY294002 group (20 µmol/L TIIA+100 ng/ml LY294002, a PI3K inhibitor). Following treatment, cellular morphology was assessed for each group using an inverted microscope. CCK8 method was used to detect cell proliferation; Flow cytometry was used to detect apoptosis in each group; the Transwell assay was used to detect cell invasion in each group; the cell scratch assay was used to detect cell migration rate, and Western blot was used to detect the expression of PI3K/AKT pathway-related proteins.

Results: Compared with the control group, the OD450 value (12,24h), the number of invasive cells and the number of migratory cells in the Schwann cells in the tanshinone IIA and the tanshinone IIA+IGF-1 groups were significantly increased (P<0.05), and the expression levels of p-PI3K, p-AKT proteins in the Schwann cells in the tanshinone IIA group was significantly increased compared with the control group P<0.05).

Discussion: This study demonstrates that Tanshinone IIA significantly enhances Schwann cell proliferation and migration while suppressing apoptosis. Crucially, these pro-regenerative effects are mediated through activation of the PI3K/AKT signaling pathway, as confirmed by inhibitor studies. These findings position Tanshinone IIA as a promising therapeutic candidate for promoting nerve repair.

Conclusion: Tanshinone IIA promotes the proliferation and migration of Schwann cells and reduces Schwann cell apoptosis by activating the PI3K/AKT pathway.