BACKGROUND: Plenty of studies have demonstrated that inflammatory reaction is involved in ischemic cerebral damage, and the expression of inflammatory cytokines can be observed at the initial sites of cerebral damage at early period, including interleukin-6, interleukin-8, etc., which are all the target gene products of nuclear factor kappa B (NF-κB). The process of ischemic damage can be affected by adjusting and controlling NF-κB activity via multi-links. OBJECTIVE: To investigate the inhibitory effect of interleukin-10 on the expression of NF-κB in the ischemic sites of rats with focal cerebral ischemia in rats and its molecular mechanisms. DESIGN: A randomized and controlled animal trial. SETTING: Department of Neurology, the Affiliated Union Hospital of Fujian Medical University. MATERIALS: Thirty-two adult male Sprague-Dawley rats weighing (250±30) g were used. NF-κB p65 (RelA) rabbit anti-rat monoclonal primary antibody was the product of Neomarkers Company; Immunohistochemical kit of the SP two-step method was purchased from Beijing Zhongshan Biotechnology Co., Ltd. METHODS: The experiment was carried out in the Affiliated Union Hospital of Fujian Medical University from August 2005 to April 2006. The rats were randomly assigned into sham-operated group, middle cerebral artery occlusion (MCAO) group, vehicle-treated group and interleukin-10 treated group, 8 rats in each group. Focal cerebral ischemia was induced by occlusion of the middle cerebral artery as previously described. Rats in the MCAO group were anesthetized intraperitoneally, thyroid was bluntly dissected. Right common, external and internal carotid arteries were isolated, the trunk of external carotid artery was ligated and freed, an artery clamp was placed at the internal carotid artery, then a “V” shape incision was made at the free section of external carotid artery, filament was inserted for a depth of (18.5±0.5) mm. The rats in the sham-operated group were given the same treatments with the exception of filament insertion. After the successful model establishment for 1 hour, the rats in the interleukin-10 treated group were injected with human recombinant interleukin-10 (1 μg) via lateral ventricle, whereas those in the vehicle-treated group were injected with 5 mol/L NaP (5 μL). The rectal temperature of rats were kept at about 37 ℃ with heating lamps throughout the operation. Twenty-four hours after MCAO, the rats were examined for neurological deficits. Only those animals that scored at 1-3 points were utilized. The rats were decapitated at 24 hours postoperatively. The expression of NF-κB p65 in peri-infarct core was detected immunohistochemically. The percentage of NF-κB p65 subunit positive cells in 1 000 cells was calculated. MAIN OUTCOME MEASURES: Expression of NF-κB p65 in peri-infarct core; Percentage of NF-κB p65 subunit positive cells. RESULTS: All the 32 rats were involved in the analysis of results. NF-κB p65 expressed in cytoplasm and some nuclei. It was expressed all in cytoplasm in the sham-operated group, and partly expressed in the nucleus after cerebral ischemia. Small amounts of NF-κB p65 positive neurocytes were observed in the sham-operated group[(3.7±0.6)%], those were obviously increased in the MCAO group [(15.4±3.7)%, P < 0.01]. NF-κB p65 positive neurocytes were significantly reduced in the interleukin-10 treated group as compared with those in the vehicle-treated groups [(12.1±2.2)%, (15.5±3.6)%, P < 0.05]. CONCLUSION: Interleukin-10 injected via lateral ventricle can effectively inhibit the expression of NF-κB p65 in the peri-ischemic core in rats, and block the gene transcription involved in the inflammatory cascade reaction. BACKGROUND: Plenty of studies have demonstrated that inflammatory reaction is involved in ischemic cerebral damage, and the expression of inflammatory cytokines can be observed at the initial sites of cerebral damage at early period, including interleukin-6, interleukin-8, etc., which are all the target gene products of nuclear factor kappa B (NF-κB). The process of ischemic damage can be affected by adjusting and controlling NF-κB activity via multi-links. OBJECTIVE: To investigate the inhibitory effect of interleukin-10 on the expression of NF-κB in the ischemic sites of rats with focal cerebral ischemia in rats and its molecular mechanisms. DESIGN: A randomized and controlled animal trial. SETTING: Department of Neurology, the Affiliated Union Hospital of Fujian Medical University. MATERIALS: Thirty -two adult male Sprague-Dawley rats weighing 250 ± 30 g were used. NF-κB p65 (RelA) rabbit anti-rat monoclonal primary antibody was the product of Neomarkers Company; Immunohistochem ical kit of the SP two-step method was purchased from Beijing Zhongshan Biotechnology Co., Ltd. METHODS: The experiment was carried out in the Affiliated Union Hospital of Fujian Medical University from August 2005 to April 2006. The rats were randomly assigned into sham -operated group, middle cerebral artery occlusion (MCAO) group, vehicle-treated group and interleukin-10 treated group, 8 rats in each group. Focal cerebral ischemia was induced by occlusion of the middle cerebral artery as previously described. Rats in the MCAO group were anesthetized intraperitoneally, thyroid was bluntly dissected. Right common, external and internal carotid arteries were isolated, the trunk of external carotid artery was ligated and freed, an artery clamp was placed at the internal carotid artery, then a “V” shape incision was made at the free section of external carotid The rats in the sham-operated group were given the same treatments with the had the successful model establishment for 1 hour, the rats in the interleukin-10 treated group were injected with human recombinant interleukin-10 (1 μg) via lateral ventricle, but those in the vehicle-treated group were injected with 5 mol / L NaP (5 μL). The rectal temperature of rats were kept at about 37 ° C with heating lamps throughout the operation. Twenty-four hours after MCAO, the rats were examined for neurological deficits. Only those animals that scored at The percentage of NF-κB p65 in peri-infarct core was detected immunohistochemically. The percentage of NF-κB p65 subunit positive cells in 1 000 cells was calculated. MAIN OUTCOME MEASURES: Expression of NF-κB p65 in peri-infarct core; Percentage of NF-κB p65 subunit positive cells. RESULTS: All the 32 rats were involved in the analysis of results. NF-κB p65 expressed in cytoplasm and some nucle i. It was expressed all in cytoplasm in the sham-operated group, and fragments expressed in the nucleus after cerebral ischemia. Small amounts of NF-κB p65 positive neurocytes were observed in the sham-operated group [(3.7 ± 0.6)%] , those were obviously increased in the MCAO group [(15.4 ± 3.7)%, P <0.01]. NF-κB p65 positive neurocytes were significantly reduced in the interleukin-10 treated group as compared with those in vehicle- treated groups [( 12.1 ± 2.2%, (15.5 ± 3.6)%, P <0.05] CONCLUSION: Interleukin-10 injected via lateral ventricle can effectively inhibit the expression of NF-κB p65 in the peri-ischemic core in rats, and block the gene transcription involved in the inflammatory cascade reaction.