The aim of this study to investigate the effects of melamine exposure from the weaning period on the developing brain in rats. Female Wistar albino rats (21 days old, n = 18) were divided into 3 groups, all animals were weighed daily and dose-adjusted. For 3 weeks, 0.1 mL of saline was administered by oral gavage to the control group, 50 mg/kg of melamine to the second group, and 75 mg/kg of melamine to the third group were administered by oral gavage by dissolving in 0.1 mL of saline. On the postnatal 45th day, the rats were sacrificed under anesthesia and brain tissues placed in neutral formalin. After routine tissue processing, brain sections were stained with hematoxylin&eosin(H&E) and Terminal deoxynucleotidyl transferase(TdT) dUTP Nick-End Labeling(TUNEL), IBA-1, Glial Fibrillar Acidic Protein(GFAP), Tumor necrosis factor-α (TNF-α), and SMI-70 antibodies as immunohistochemically. In the results, according to apoptotic index(AI) results, there was a significant increase in the 75 mg/kg and 50 mg/kg melamine groups compared to the control groups (p < 005). There was a significant increase in the number of anti- TNF-α positive neurons and the number of anti-GFAP positive astrocytes in both melamine groups compared to the control group (p < 001). In terms of SMI-71, an increase was found in the 75 mg/kg group compared to other groups (p < 001), while no significant difference was found between the groups in terms of IBA-1 (p > 0.05). It has been observed an increase in dilatation of blood vessels, inflammatory cell infiltration, and endothelial cell degeneration in the 50 mg/kg and 75 mg/kg melamine groups compared to the control group (p < 0.01). there was no statistically significant difference in the body and brain weight between both melamine treatment groups (75 mg/kg and 50 mg/kg) and the control group (p > 005). Melamine exposure (50 mg/kg and 75 mg/kg) from the weaning period causes apoptosis and inflammation in the developing brain, and the disruptions in the blood-brain barrier (BBB) significantly increase exposure to 75 mg/kg.

本研究的目的是调查断奶期接触三聚氰胺对大鼠大脑发育的影响。女威斯塔白化大鼠（21 天大，n = 18）分为 3 组，所有动物每天称重并调整剂量。3周内，对照组灌胃0.1毫升生理盐水，第二组灌胃50毫克/公斤三聚氰胺，第三组灌胃75毫克/公斤三聚氰胺，溶解于0.1毫升生理盐水。出生后第45天，麻醉处死大鼠，脑组织置于中性福尔马林中。常规组织处理后，脑切片用苏木精&伊红（H&E）和末端脱氧核苷酸转移酶（TdT）dUTP Nick-End Labeling（TUNEL）、IBA-1、胶质纤维酸性蛋白（GFAP）、肿瘤坏死因子-α（TNF- α) 和 SMI-70 抗体作为免疫组织化学。结果中，根据凋亡指数（AI）结果，与对照组相比，75 mg/kg 和 50 mg/kg 三聚氰胺组显着增加（p < 005）。与对照组相比，两个三聚氰胺组的抗 TNF-α 阳性神经元数量和抗 GFAP 阳性星形胶质细胞数量均显着增加（p < 001）。在 SMI-71 方面，75 mg/kg 组与其他组相比有所增加（p < 001），而在 IBA-1 方面，各组之间没有发现显着差异（p > 0.05）。已经观察到，与对照组相比，50 mg/kg 和 75 mg/kg 三聚氰胺组的血管扩张、炎症细胞浸润和内皮细胞变性增加（p < 0.01）。三聚氰胺治疗组（75 毫克/公斤和 50 毫克/公斤）和对照组之间的体重和大脑重量没有统计学上的显着差异（p > 005）。从断奶期开始接触三聚氰胺（50 毫克/千克和 75 毫克/千克）会导致发育中的大脑发生细胞凋亡和炎症，血脑屏障 (BBB) 的破坏显着增加了 75 毫克/千克的接触。