[en] Objective: To investigate the rule of the aquaporin-4 (AQP-4) expression in the acute ischemic cerebral tissues, and to study the molecular biologic mechanism of diffusion-weighted imaging (DWI). Methods: Thirty-six Wistar rats were divided into 2 groups randomly, including control group (n=12) and operation group (n=24). The operation group was studied after the right middle cerebral artery was unilaterally occluded (MCAO) at an interval of 15 min, 30 min, 1 h, 3 h, 6 h, and 24 h, respectively (n=4 for each sub-group). The operation process of the control group was the same as the operation group except MCAO. All rats in both groups were examined with DWI. The relative ADC (rADC), relative density (rd), and relative area (rs) of the biggest hyperintensity signal layer on DWI were measured. After that, the animals were sacrificed and perfused with the mixture solution consisting of TTC at different time intervals. The biggest layer of the ischemic cerebral tissues stained with TTC and corresponding to that of DWI was examined with immunochemistry and in situ hybridization. The AQP-4 expression AQP-4 (ΔS and α) was measured with the Image Analyzer. Meanwhile, histologic examination was performed at each group. Results: There was no significant change of the DWI and the pathology, as well as the AQP-4 expression in the control group. In the operation group, abnormal high intensity was found in DWI of ipsilateral MCA territory at 15 min after MCAO, and rADC value decreased quickly within 1 h after MCAO, while the AQP-4 expression, the rd-DWI, and the rs-DWI increased rapidly in the stage. With the progress of the time, the rADC value further decreased at 3 h, and then began increasing slowly till 24 h. But the AQP-4 expression (ΔS and α) and the rd as well as the rs continuously increased slowly between 1 h and 6 h after MCAO, then they had an increasing peak except the rd. The AQP-4 expression, rd-DWI, and rs-DWI all showed positive linear relationship with time, presenting as 2 peaks and a plateau. The corresponding sequential pathologic changes were gradual increase of intracellular edema (<1 h) , then emergence of vasogenic and cytotoxic edema (1-6 h) , and final necrosis and liquefaction (6-24 h). Conclusion: The high expression of AQP-4 in the acute ischemic cerebral tissues played a significant role in the intracellular edema. Certainly, it was also one of the important reasons of the decrease of rADC and hyperintensity on DWI in the early stage of the cerebral ischemia