目的通过建立大鼠脑梗死模型,探讨白细胞介素-23(IL-23)在大鼠脑梗死区域炎性损伤中的表达。方法 (1)将健康成年雄性SD大鼠50只随机分为脑梗死组和假手术组,每组25只。脑梗死组按梗死后不同取材时间分为6、24、48、72h及7d 5个亚组,每组大鼠5只;假手术组按梗死组对应时间点分为6、24、48、72h及7d5个亚组,每组大鼠5只。(2)用线栓法制作左侧大鼠大脑中动脉阻塞(MCAO)模型。(3)采用HE、免疫组化染色,观察脑梗死区域光镜下形态学变化及IL-23的表达。(4)比较两组大鼠在同一时间点脑组织形态学变化及IL-23的表达。结果 (1)假手术组各时间点脑组织结构基本正常,无明显水肿。脑梗死组MCAO术后6h脑组织病变区域脑组织轻度水肿。24～48h水肿加重;(2)梗死组IL-23阳性细胞个数各时间点均高于假手术组,差异有统计学意义(P<0.01)。梗死组IL-23随时间的延续变化,在梗死后6h表达增高,并且在梗死后48h达到高峰,72h后阳性细胞数表达逐渐减少,各时间点IL-23比较差异有统计学意义(P<0.001)。结论 IL-23在大鼠脑梗死区域表达均显著增高,而且在24～48h达高峰。 Objective To investigate the expression of interleukin-23 (IL-23) in the inflammatory injury of cerebral infarction in rats by establishing a rat cerebral infarction model. Methods (1) 50 healthy adult male SD rats were randomly divided into cerebral infarction group and sham operation group, 25 rats in each group. The cerebral infarction group was divided into 5 subgroups of 6, 24, 48, 72h and 7d according to the different time after infarction, 5 rats in each group. The sham operation group was divided into 6, 24, 48 and 72h according to the corresponding time point of infarction group And 7d5 subgroups, 5 rats in each group. (2) Left middle cerebral artery occlusion (MCAO) model was made by thread occlusion. (3) HE and immunohistochemical staining were used to observe the morphological changes and the expression of IL-23 under light microscope in the infarcted area. (4) The brain morphological changes and the expression of IL-23 in the two groups were compared at the same time point. Results (1) At each time point in sham operation group, the brain tissue structure was basically normal with no obvious edema. Cerebral infarction group MCAO 6h brain tissue lesion area mild edema. (2) The number of IL-23 positive cells in infarction group was higher than that in sham operation group at each time point, the difference was statistically significant (P <0.01). The expression of IL-23 in infarction group changed with time and increased at 6h after infarction, and peaked at 48h after infarction. The expression of IL-23 decreased gradually after 72h, and the difference was significant at each time point (P < 0.001). Conclusion The expression of IL-23 in cerebral infarction area of ​​rats were significantly increased, and reached the peak at 24 ~ 48h.