Objective To investigate the effect of kindlin‑1 on astrocyte activation in the spinal cord of rats with neuropathic pain. Methods A total of 18 male 10‒12‑week‑old SD rats, weight 250‒280 g, were divided into three groups according to the random number table method (n=6): a sham operation group (group S), a neuropathic pain group (group NP) and a kindlin‑1 inhibition group (group K). A neuropathic pain model was established by chronic constriction of the sciatic nerve. The sciatic nerve of group S was only being exposed without ligation. Rats in group K were intrathecally injected with short hairpin RNA (shRNA) 21 d before surgery to inhibit the expression of kindlin‑1. Those in groups S and NP were intrathecally injected with viral vector 21 d before surgery for control. The paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured 1 d before surgery and 1, 4, 7, 10 d and 13 d after surgery, respectively. When pain threshold measurement finished 13 d after surgery, the rats were sacrificed to collect the spinal cord tissue. The expression of kindlin‑1 and astrocytes were detected by immunofluorescent double staining. Also, the expression of kindlin‑1 in the spinal cord was measured by Western blot. Results Compared with group S, rats in group NP had reduced PWMT and shortened PWTL as well as up‑regulated expression of kindlin‑1 protein in the spinal cord 4, 7, 10 d and 13 d after surgery. Meanwhile, increases in optical density (D) value of kindlin‑1 and astrocyte activation rate were also seen in group NP (P<0.05). Compared with group NP, group K had increased PWMT and extended PWTL as well as down‑regulated expression of kindlin‑1 in the spinal cord 4, 7, 10 d and 13 d after surgery. Meanwhile, decreases in D value of kindlin‑1 and astrocyte activation rate were seen in group K (P<0.05). Conclusions Kindlin‑1 is involved in the activation of astrocytes in the spinal cord of rats with neuropathic pain.