Inhibition of Wnt/β-catenin signal is alleviated reactive gliosis in rats with hydrocephalus.

BACKGROUND

Reactive gliosis has been implicated in the pathogenesis of communicating hydrocephalus. Because the activation of Wnt/β-catenin signaling pathway is considered as a significant factor to contribute to brain development, neurodegenerative process, and reactive gliosis, we target this pathway for intervention by using sFRP-l and investigated the expression of β-catenin, cyclin D-1, and glial fibrillary acidic protein (GFAP) in the brain of experimental hydrocephalic rats in terms of protein and gene expression.

METHODS

Therefore, 30 adult SD rats were randomly divided into the normal group (n = 5), the sham operation group (n = 5), the hydrocephalus group (n = 10), and the sFRP-l group (n = 10). Hydrocephalic rat models were induced by intraventricular injections of 3% kaolin while sFRP-l group was treated by sFRP-l with kaolin injections. The ventricular dilatation was examinated by MRI at 2-week post-operation. After that, β-catenin, cyclin D-1, and GFAP were qualified by Western blot and immunohistochemistry.

RESULTS

According to the result, the expression of β-catenin and cyclin D-1 increased (P < 0. 05) in the brain tissue of the hydrocephalus group compared with that of the sham group, while GFAP expression in the hydrocephalus group is more obvious (P < 0. 05). In the sFRP-l group, the expression of β-catenin and cyclin D-1 and GFAP expression is lower (P < 0. 05) compared with those of the hydrocephalus group. We demonstrated that the Wnt/β-catenin pathway is activated in the experimental hydrocephalic rat brain. sFRP-l inhibited the expression of β-catenin and cyclin D-1 and alleviated reactive gliosis in the hydrocephalic rat brain tissue, while the development of hydrocephalus was delayed.

CONCLUSION

These results suggest that regulating Wnt/β-catenin signaling pathway may provide new therapeutic methods for hydrocephalic patients.