BACKGROUND: Previous studies have focused on gene expression acutely following stroke onset. However, there have been a few reports of gene expression during later stages of cerebral infarction. OBJECTIVE: To determine gene expression profiling in the peri-infarct brain cortex 7 days after ischemia in a rat model of cerebral infarction in renovascular hypertensive rats. DESIGN, TIME AND SETTING: An in vivo, molecular experiment was performed at the Experimental Animal Center of Sun Yat-sen University and CapitalBio, Beijing, China between February 2004 and August 2005. MATERIALS: A 70-mer oligo chip containing 5 705 rat genes was supplied by CapitalBio, Beijing, China; and the Oligo rat gene bank was provided by Qiagen, the Netherlands. METHODS: Six Sprague Dawley rats were utilized to establish a stroke-prone renovascular hypertensive model using the two-kidney and two-clip method. The rats were subsequently randomly assigned to two groups: middle cerebral artery occlusion and sham-operation, with three rats in each group. The middle cerebral artery occlusion model was induced by intraluminal suture method. Incisions were sutured following isolation of carotid arteries in the sham-operation group. MAIN OUTCOME MEASURES: Total RNA was extracted from the peri-infarct cerebral cortex 7 days after surgery. Following fluorescent labeling, RNA was hybridized to an Oligo chip containing 5 705 genes and was then scanned. Images were collected and the differentially expressed genes (number and category) were selected by data analysis. RESULTS: A total of 174 genes were upregulated, and 23 were downregulated, in the peri-infarct cerebral cortex 7 days after ischemia. The upregulated genes were distributed among 12 functional categories, and the downregulated genes belonged to categories of transport, transcription regulators, signals, response to stress, metabolism, and cell adhesion. The expression of some cytoskeletal genes was upregulated, including VIM, A2M, B2M, ACTR3, and ARPC1B. Expression of a few cell adhesion-related genes (such as NLGN1, LGALS1, LGALS3, COL1A1, COL2A1, and SPP1) and other inflammation-related genes (such as C1QB, C1S, C4, C5R1, CFH, CD14, CD164, CD47, CD48, CD53, CD8B, IFNGR, and TFITM2) were upregulated. The glutamate-receptor gene GRIK5 was downregulated, which is related to the excitatory neurotransmitter glutamate. However, expression of the inhibitory neurotransmitter GABA-related genes was bidirectional - namely, GABRA5 downregulation and GABARAP upregulation. CONCLUSION: Upregulation of many cell adhesion and inflammation related genes and downregulation of excitatory glutamate-related receptor genes revealed active gene expression during later stages of cerebral infarction, which suggested molecular mechanisms of injury or repair.