Objective To investigate the influence of signal transducer and activator of transcription 3 (STAT3) on neural cell injury caused by intracerebral hemorrhage (ICH) by regulating the sonic hedgehog (Shh) signaling pathway. Methods Rat neuron PC12 cells were divided into control group and ICH model group, and qRT-PCR and Western blot were used to measure the mRNA and protein expression levels of STAT3 and Shh. MTT assay was used to analyze the proliferation curve of cells in the two groups, and flow cytometry was used to measure cell apoptosis rate. BALB/c mice were randomly divided into sham-operation group, ICH model group, ICH+PBS group, and ICH+Stattic (STAT3 inhibitor) group. HE staining was used to assess brain injury in each group of mice. The RNA interference technique was used to silence the expression of STAT3 in PC12 cells or transfect overexpression vectors to increase the expression of Shh, and MTT assay and flow cytometry were used to measure the changes in the proliferation curve and apoptosis of PC12 cells. Results The ICH group showed significant increases in the mRNA and protein expression levels of STAT3 (P<0.05) and significant reductions in the mRNA and protein expression of Shh in brain tissue (P<0.05). Inhibition of STAT3 alleviated brain injury in ICH mice. After STAT3 was silenced, there were significant increases in the expression of Shh signal-related proteins (Shh, SMO, and Gli-1) in ICH model (P<0.05), and there was a significant increase in the proliferation of PC12cells (P<0.05) and a significant reduction in the apoptosis rate of PC12 cells (P<0.05). Overexpression of Shh promoted the proliferation of PC12 cells in IHC model (P<0.05) and reduced cell apoptosis (P<0.05). Conclusions STAT3 influences the proliferation and apoptosis of PC12 cells in ICH cell model by regulating the Shh signaling pathway.