Objective To explore the effect of STAT3 regulating Shh signaling pathway on nerve cell defect caused by cerebral hemorrhage (ICH). Methods PC12 cells were divided into control group and ICH model group. The expression levels of STAT3 and Shh were detected by qRT-PCR and western blot. Cell proliferation level was detected by MTT assay. Apoptosis rate was detected by flow cytometry. BALB/c mice were randomly divided into sham group, ICH model group, ICH+PBS group and ICH+Stattic (STAT3 inhibitor) grou. The brain injury of mice in each group was detected by HE staining. Interference RNA technology silenced the expression of STAT3 in PC12 cells or transfected expression vectors to increase the expression of Shh. MTT and flow cytometry were used to detect the proliferation and apoptosis of PC12 cells. Results In ICH group, the expression level of STAT3 increased in cells and mice (P<0.05), while the expression of Shh decreased (P<0.05). Inhibition of STAT3 reduced the brain damage in ICH mice. After silencing STAT3, the expression of Shh signal-related protein (Shh，SMO and Gli-1) in ICH model were increased (P<0.05), the proliferation of PC12 cells increased (P<0.05) and the apoptosis rate decreased (P<0.05). Overexpression of Shh promoted the proliferation of PC12 cells in IHC model (P<0.05) and reduced the apoptosis (P<0.05). At the same time, knocking down Shh could reverse the effect of knocking down STAT3 on ICH model cells. Conclusions STAT3 regulated Shh signaling pathway and regulated PC12 cell proliferation and apoptosis in ICH cell model.