ALO alleviated the long‐term neurobehavioral deficits caused by HI insult; reduced the extent of cerebral infarction; inhibited cell apoptosis; decreased the levels of the inflammatory factors interleukin (IL)‐1β, IL‐6, and tumor necrosis factor‐α; activated microglia and astrocytes; and downregulated the protein expression of members in the TLR4 signaling pathway. The gene discussed is TLR4; the disease is cerebral infarction.