Zinc （Zn2+） has both neurotoxic and neuroprotective capabilities which is related to the homeostasis of Zn2+ in the brain. Labile Zn2+ plays a catalytic role mainly through zinc transporters， zinc finger proteins and some other proteins， and participates in hundreds of physiological processes including autophagy. Cerebral ischemic injury induces the pathological release of Zn2+， which may ultimately cause cell death by inducing excessive neuronal autophagy. The disorder of autophagy also causes abnormal metabolism of Zn2+. This review aims to discuss the interaction and reciprocal regulation between Zn2+ and autophagy during cerebral ischemia injury.