Objective To investigate the effect of tumor necrosis factor receptor 1 （TNFR1） in angiogenesis and neurogenesis during cerebral ischemia in mice. Methods Twenty-four wild-type and 24 TNFR1 knockout mice were randomly divided into either a sham operation group or a focal cerebral ischemia group （n = 12 in each group）. 5-bromodeoxyuridine （BrdU） was injected intraperitoneally at day 3 after cerebral ischemia and sham operation. At day 7 and 28 after cerebral ischemia, the double-label immunofluorescence staining of glucose transporter-1 （Glut-1）/BrdU was used to evaluate the angiogenesis surrounding the areas of infarction. A labeled BrdU was used to detect the neural stem cell proliferation in the subventricular zone. Double-labeled doublecortin （DCX）/BrdU and neuronal nuclei antigen （NeuN）/BrdU were used to detect the migration and survival of neural stem cells, respectively. Results Under the normal condition, there was no significant difference in angiogenesis and the number of BrdU-positive cells in the subependymal zone （SVZ） between the wild-type （418. 000 ±28. 404） and TNFRI knockout （528. 000 ±60. 597） mice （t = - 1. 644, P =0. 131）. At day 7 after cerebral ischemia, the number of Glut-1/BrdU-positive cells in the TNFR1 knockout mice was significantly less than that in the wild-type mice （14. 833 ±2. 182 vs. 27.5 ±4. 209） （t =2. 672, P=0. 023）, and the number of DCX/BrdU-positive cells was also significantly less than that in the wild-type mice （163. 000± 11. 106 vs. 257. 168 ±12. 213） （t = 5. 705, P = 0. 000）. At day 28 after cerebral ischemia, the number of NeuN/BrdU-positive cells in the TNFR1 knockout mice was significantly less than that in the wild- type mice （6. 000 ±0. 577 vs. 11. 000 ±1. 571） （t = 2. 988, P = 0. 014）. Conclusions TNFR1 may play a promoting role in the neurovascular regeneration in late cerebral ischemia.