Interleukin‑1β (IL‑1β) is a pleiotropic cytokine that mediates inflammatory and cell death activities. IL‑1β has been previously reported to induce apoptosis of intervertebral disc (IVD) cells in IVD degeneration. Accumulating data have suggested that post‑menopausal women have a high incidence of IVD degeneration. It has therefore been proposed that estrogen may have a close association with IVD degeneration. Whether estrogen is able to protect IVD cells from apoptosis remains unclear. The present study aimed to examine whether 17β‑estradiol (17β‑E2) inhibited IL‑1β‑induced apoptosis of rat annulus fibrosus (AF) cells. Additionally, the dose‑response effect of 17β‑E2 on cell apoptosis was investigated. AF cells were isolated from male Sprague Dawley rats and cultured in complete medium. Following approximately two weeks, the AF cells were treated with IL‑1β (75 ng/ml) for 24 h, with a pretreatment of 17β‑E2 for 1 h. Apoptosis of AF cells was analyzed by annexin V/propidium iodide binding assay and morphological changes, together with an assessment of caspase‑3 activity. Cell viability of the AF cells was determined by MTT assay. The level of apoptosis and caspase‑3 activity in the AF cells was increased whereas the cell viability was decreased following treatment with IL‑1β (75 ng/ml), as compared with the control group. This effect was reversed by pretreatment with 17β‑E2, in a dose‑dependent manner. The protective effect of 17β‑E2 was abolished by estrogen receptor antagonist ICI182, 780. These results indicate that 17β‑E2 protects rat AF cells from apoptosis induced by IL‑1β, in a dose‑dependent manner.